Internal Medicine II Neurology cases

Scenario N1: Fatigue and lethargy (key symptom) accompanied by fever, headache irritability. Neurological symptoms that can potentially develop ataxia, hemiplegia, seizures, inflammation of the optic nerve (optic neuritis) scenario N2: All above +/ only pilot/aircraft man, no measles vaccine made

Localisation: The leptomeningies(pia and arachnoid matter),Brain parenchyma And if spine is affected,spinal cord tissue Diagnosis-Aseptic Meningoencephalitis *If it's a "Pilot or Aircraft man" + "Measles vaccine" = Dx: ADEM optic nerve (optic neuritis) Differential diagnosis: 1.Meningoencephalitis 2.Meningoencephalomyelitis 2. ADEM-acute disseminated encephalomyelitis,it is monophasic lesion in white matter of the tissue of brain and spinal cord)-common in child hood, inflammation and loss of white matter, There's no relapse or remission in ADEM unlike Multiple sclerosis 3. Viral(Aseptic) Meningitis 4. Lethargic Encephalitis 5.Tick borne Encephalitis Lab Diagnostic tests: Blood tests,lumbar puncture, PCR test for viral suspicion, csf culture,MRI. 1. MRI 2. Lumbar puncture(csf protein is normal or mildly elevated) Treatment: for our case, acyclovir, Famciclovir, for up to 14 days to treat aseptic Meningoencephalitis. 2. Normalize vital functions,Dehydration and deintoxification 3. Dexomethasone to reduce inflammation, 4.Corticosteroids, and diuretics to lower pressure and swelling or inflammation in brain 5.NSAIDs to reduce pain 6.Phenytoin to prevent seizures Prognosis-Unfavorable,nearly 50 to 70% of people will develop secondary brain damage, coma or neurological (nerve) disorders if not treated as an emergency Side note- Meningoencephalitis is a very serious neurological condition resembling both meningitis and encephalitis - inflammation of the meninges (covering of the CNS) and inflammation of the brain tissues respectively. "Encephalitis": inflammation of the brain tissue Depending on the structure of the brain tissue that is affected, encephalitis can be divided into: 1. Leukoencephalitis: inflammation of the white matter of the brain. 2. Polio encephalitis: inflammation of the grey matter of the brain. 3. Panencephalitis: inflammation of both white & grey matter of the brain. Meningoencephalitis can be caused by bacteria, viruses, fungi, and protozoan or as secondary sequel of other inflammations like AIDS. The viral or aseptic meningoencephalitis is mainly caused by enteroviruses, varicella-zoster viruses, herpes simplex viruses. The main goals of treating meningoencephalitis are to treat the symptoms and the cause of inflammation: Give IV Antibiotics and IV antiviral medication such as acyclovir, Famciclovir, for up to 14 days if it's HSV. Do empirical treatment before culture is obtained (3rd gen cephalosporins, IV ceftriaxone 4mg, menorem 3mg/ Day,Acyclovir & Famciclovir) Broad spectrum antibiotics covering gram positive and negative bacteria and antiviral meds Treat according once culture is certain

45yo male, car accident, conscious but sedated, due to severe back ache, he shows both sensory and pathologic weakness of left upper limb along with loss of tendon reflex, central palsy in left lower limb. On opposite side loss of pain, temp and tactile.

Localization: Hemi-section of spinal cord at the level of C5-C6, on the left side (presenting as Brown- Sequard syndrome) Diagnosis: spinal cord trauma case comments N1: Brain trauma types: 1. Concussion - depends on location eg. concussion of frontal lobe - reversible damage to brain parenchyma (lasts no more than 1-20mins) 2. Contusion - depending on location eg. contusion of frontal lobe - damage to brain parenchyma (longer periods of unconsciousness and amnesia) 3. Compression 4. Epidural haematoma - traumatic tearing of Dural artery (usually middle meningeal artery), results in temporal-parietal skull fracture - blood accumulation between periosteum and dura mater 5. Subdural haematoma - blood accumulation between dura mater and arachnoid mater, due to bridging veins tear 6. Post-concussion syndrome - cerebral and subcortical structure lesion

That is malignant tumor derived from the granular cells of the cerebellum (neuroectoderm). • Usually arises in children • Histology reveals small, round blue cells; Homer-Wright rosettes may be present. • Poor prognosis; tumor grows rapidly and spreads via CSF 1. Metastasis to the cauda equina is termed 'drop metastasis.

Medulloblastoma

Other questions for basic knowledge N1: Most common CNS tumor in children. That tumor arises in the cerebellum • Imaging reveals a cystic lesion with a mural nodule. • Biopsy shows Rosenthal fibers (thick eosinophilic processes of astrocytes, and eosinophilic granular bodies; tumor cells are GFAP positive.

Pilocytic astrocytoma

That tumor may occur at any age Occur at any age, but are most common in childhood and especially in boys. If the tumor compresses: • The aqueduct of Sylvius - it causes hydrocephalus, papilledema and other signs of increased intracranial pressure • The pretectum rostral to the superior colliculi - it causes paralysis of upward gaze, ptosis, loss of pupillary light and accommodation reflexes

Pineal tumours (usually germinomas)

a 75-year-old man presents with resent onset loss of movement of his right arm. the right side of his face also droops and there is drooling from the corner of his mouth on the right side. he has difficulty of speaking. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localisation: middle and lower part of the precentral gyrus of frontal lobe on left side+broca's area diagnosis": MCA ischemic stroke on left side case comments N1: *middle and lower part of the precentral gyrus- weakness in arm(middle) and face(lower) *damage to Broca's area(in frontal lobe)- difficulty speaking Differential diagnosis: 1. MCA ischemic stroke 2. MCA hemorrhagic stroke 3. intracerebral hemorrhage 4. subarachnoid hemorrhage 5. frontal lobe tumor case comments N2: *frontal lobe tumors(meningioma, gliomas and oligodendrocytomas) *the Broca's area of frontal lobe is blood supplied by "middle cerebral artery". therefore, whenever patient has difficulty speaking, "MCA stroke" is most likely to be the correct diagnosis Lab diagnostic tests: CT/MRI with angiogram Treatment: 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin

Extreme back pain Initial symptom is partial or complete spinal cord transection syndrome. Stable segmentary and conductive sensory disorders. Bladder dysfunction, paraparesis or tetraparesis with following trophic disorders.

localisation: spinal cord tissue of affected area diagnosis: Spinal Cord Contusion case comments N1: Pathology: Traumatic destruction of spinal cord tissue by direct mechanical compression or haemorrhage *partial or complete spinal cord transection syndrome is depending on extent of the lesion. *Stable segmentary and conductive sensory disorders (dissociative anaesthesia). *The transection syndrome usually improves no more than partially. Differential Diagnosis: Transverse myelitis Extramedullary tumour Spinal cord compression/concussion case comments N2: Causes: Dislocated fracture Free bony fragment Herniated disc Repositioned subluxation of vertebra Diagnostic Tests: MRI, CT or X-ray of spinal cord P rognosis and Treatment: early recovery of sensation seems to be a favourable prognostic sign for motor recovery. Surgery to correct underlying cause.

Headache Epileptic seizures Focal neurological symptoms that progress over the course of few hours Evidence of intracranial hypertension - papilledema

localization depending of type: 1. Subdural haemorrhage 2. Thrombosis of deep veins 3. Intracerebral haematoma 4. Sinus thrombosis Diagnosis: Venous stroke Diagnostic tests: best done with CT venography + contrast medium (but most important diagnostic technique for evaluation of venous outflow of the brain is MRI). Differential diagnosis: All types of venous strokes: 1. Subdural Hemorrhage 2. Thrombosis of Deep Veins 3. Sinus Thrombosis 4. Intracerebral Hematoma and arterial strokes: ischemic: 5. Embolic 6. Nonembolic(thrombosis) 7. Occlusion of Magistral arteries hemorrhagic: 8. Epidural 9. Subarachnoid 10. Intraparenchymal 11. Intraventricular 12. Intracerebral and 13. Epilepsy

presentation: ptosis with horizontal gaze problem, contralateral hemiplegia 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: damage to the base of the brainstem at the level of peduncles(midbrain)-affecting CN3(presenting Weber's syndrome) diagnosis: posterior cerebral artery ischemic stroke on the contralateral side case comments N1: *presenting as Weber's syndrome *ipsilateral CN3 palsy *gaze "down and out" *ptosis(droopy eyelid) *mydriasis(eyes stay dilated when light is shined) *contralateral hemiplegia due to damage to corticospinal tract(based on the info provided we can not determine if there is contralateral hemiplegia on the opposite side of the lesion, but possibly right, due to it showing weber's syndrome symptoms) differential diagnosis: 1. PCA Ishcemic stroke 2. PCA hemorrhagic stroke 3. subarachnoid hemorrhage 4. brainstem tumor diagnostic tests: CT with angiography/MRI treatment: TEEL 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) 0.4 mg 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin

influenza virus+ coffee cup+ knife, acute symmetrically ascending weakness 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: degeneration of myelin sheath (schwann cells) of peripheral nerves- leading to polyneuropathy affecting multiple peripheral nerves = polyneuritis/polyneuropathy diagnosis: Guillain-Barre syndrome(GBS) differential diagnosis: 1. ALS- Amyotrophic lateral sclerosis- is degeneration or deterioration of anterior horn causing muscle palsy. UMN: spastic paralysis of muscles, pseudo bulbar palsy, LMN: flaccid paralysis of muscles. (hyperreflexia with hypotonia) 2. ADEM-Acute disseminated encephalomyelitis- Perivenous inflammation- loss of white matter to vessels, Monophasic lesions in white matter (antigenic challenge) 3. Botulism-descending type of paralysis 4. Multiple sclerosis-destruction of oligodendrocytes forms plaques within white mater of brain and spinal cord - common sites = Optic nerve, lateral and posterior columns, Midbrain, pons, cerebellum 5. Intramedullary tumor-manifestations- 1. No pain is observed due to the damage of posterior horn and thus loss of superficial sensation - loss of pain and temperature sensation. 2. It may affect the anterior horns and thus peripheral palsy is observed according to the place of damage. and lateral colum(lateral corticospinal)(bulbar palsy) Spinal cord compression-causing either braun sequard,Transection etc case comments N1: GBS- rare disorder in which your body's immune system attacks your nerves. Weakness and tingling in your hands and feet are usually the 1st symptoms. these sensations are quickly spread, eventually paralyzing your whole body. In its most severe form, Guillain-barre syndrome is a medical emergency. Most people with the condition must be hospitalized to receive treatment. the exact cause of GBS is unknown, but 2/3 if patients report symptoms of an infection in the 6 weeks preceding. These include a COVID-19, respiratory or GI infection, or Zika virus GBS often begins with tingling and weakness starting in your feet and legs and spreading to your upper body and arms. some people notice the 1st symptoms in the arms or face. as GBS progresses, muscle weakness can turn into paralysis case comments N2: signs and symptoms of GBS: *pins and needles sensation in your finger, toes, ankles or wrists *weakness in your legs that spreads to your upper body *unsteady walking or inability to walk or climb stairs *difficulty with facial movements, including speaking, chewing, or swallowing *double vision or inability to move the eyes *severe pain that may feel achy, shooting, or cramp-like and may be worse at night *difficulty with bladder control or bowel function *rapid RR *low or high BP *difficulty breathing *Patients with GBS usually experience their most significant weakness within 2 weeks after symptoms begin *decrease reflexes *symmetrical ascending weakness *peripheral loss of sensation *neuropathic pain *facial nerve weakness case comments N3: causes of GBS: the exact cause is unknown. The disorder usually appears days or weeks after a respiratory or digestive tract infection(such as campylobacter jejuni, cytomegalovirus, ebstein-barr virus). Most commonly campylobacter (commonly seen in undercooked poultry). Viral causes include influenza, HIV, EBV, hepatitis, and zika virus. Rabies vaccine. Rarely, recent surgery or vaccination can trigger Guilain-barre syndrome. In GBS the nerves protective myelin sheath is damaged. damage prevents nerves from transmitting signals to your brain, causing weakness, numbness, or paralysis diagnosis: history, neurological exam: 1. spinal tap(lumbar puncture). a small amount of fluid is withdrawn from the spinal canal in your lower back. 2. electromyography- thin-needle electrodes are inserted into the muscles your doctor wants to study. the electrodes measure nerve activity in the muscles. 3. nerve conduction studies. electrodes are taped to the skin above your nerves, a small shock is passed through the nerve to measure the speed of nerve signal Prognosis and Treatment: favourable prognosis. Most people fully recover Urgent hospitalisation-respiratory support if needed/thrombo emboli prophylaxis Plasmapheresis and IV gammaglobulin Complication: ascending type of Landry's paralysis (flaccid paralysis of respiratory muscles and a bulbar group of muscles (9,10,12)). Unfavorable prognosis. Treatment: Artificial respiration, steroids, and plasmapheresis. case comments N4: Signs: Areflexia Paraesthesia's Shocklike, tingling pain (which is misattributed to disc herniation, flu, or rheumatism). Symptoms on both sides Symptoms appear quickly (days or weeks instead of months) Bilateral CN 7 peripheral palsy Landrys paralysis-bulbar palsy(CN 9,10,12) and rapid ascending paralysis affecting the respiratory system causing diaphragmal palsy Recovery (remyelination and axonal growth) beginning within 4 weeks after progression stops. Sensitivity improves first followed by motor function and then reflex disorders disappear. Epidemiology: More common in those with Hodgkins lymphoma. Symptoms: Acute ascending rapid onset of progressive symmetrical bilateral weakness of lower limbs. Sometimes spreads to upper limbs, causing respiratory muscle weakness. Blood pressure and heart function affected (autonomic disturbances) pathophysiology of GBS: B cells of the immune system create antibodies against the infective pathogen and this antibodies also damage proteins of the peripheral nerve cells. 1. 4 weeks- GI symptoms 2. symptoms starts from feet 3. 2-4 weeks- symptoms peak 4. months-years- recovery period case comments N5 Amyotrophic lateral sclerosis (Lou Gehrig disease) disease confined to the corticospinal tracts and the motor neurons of the anterior gray columns of the spinal cord. It is rarely familial and is inherited in about 10% of patients. Most cases are sporadic, arising in middle age adults due to "Zinc-copper superoxide dismutase mutation (SOD/) is present in some familial cases that leads to free radical injury in the neurons. Amyotrophic lateral sclerosis is a chronic progressive disease of unknown etiology. Typically, it occurs in late middle age and is inevitably fatal in 2 to 6 years. The anterior motor horn degeneration leads to lower motor neurons signs: • Seen together with bulbar palsy • Flaccid paralysis with muscle atrophy • Fasciculations and weakness with decreased muscle tone • Impaired reflexes • negative Babinski sign • weakness or atrophy and occasionally fasciculations Lateral corticospinal tract degeneration leads to upper motor neuron signs: • seen together with pseudobulbar palsy • Spastic paralysis with hyperreflexia • Increased muscle tone • Positive Babinski sign • Clumsiness, stiffness, and fatigue The lower motor neuron signs of progressive muscular atrophy, paresis, and fasciculations are superimposed on the signs and symptoms of upper motor neuron disease with paresis, spasticity, and Babinski response. The motor nuclei of some cranial nerves may also be involved. Treatment only benzothiazole and riluzole has been shown to extend lifespan.

a girl who was in car accident and rib cage damage, spleen damage, all dermatomes gone from abdomen and below 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: spinal cord compression(transverse dissection) at the level T6 and below Diagnosis: spinal cord compression due to trauma *intercostal innervation is at the level T6 differential diagnosis: 1. transverse myelitis 2. intramedullary tumor 3. extramedullary tumor 4. spinal cord hematoma Diagnostic tests: 1. Neurological exam(to determine level of lesion) 2. lubmar puncture(to observe potential blood) 3. X-ray, Ct and MRI Treatment: 1. immobilization 2. surgical removal of bony fragments 3. pain-relief(analgesics, NSAIDs) 4. vitamin B12 5. rehabilitation

- lateral hemisection in spinal cord in left side, segment C5-C8 damage. what will be observed?

- According to damage of anterior horn of this level which are correspond for innervation of upper extremities and according to damage observe peripheral palsy of left upper limb. - According to damage to posterior horns of this level will observed, spinal segmental Syringomyelic dissociation in left dermatomes which are innervated by C6-C7. On the side below the level: - According to damage to posterior column on this side and below process (below last affected segment C8) will find spinal conductive Tabetic dissociation below the upper limb, in the lower limb . - According to damage to lateral column on this side and below damage to lateral corticomuscular tract will observed central palsy on the left lower limb On the opposite side and below the level: - According to damage to lateral column, thoracic T2-T3 and below, will find spinal conductive syringomelinic dissociative on opposite side in lower limb.

tremor in hand, paralysis in leg. EEG is normal 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: irritation of precentral gyrus(upper and middle part) of the frontal lobe Diagnosis: motor(jackson) epilepsy *in "Todd's paralysis"(usually only affects one side of the body) of the lower limb remain weak for some hours before returning to normal Differential diagnosis: 1. motor(jackson) epilepsy 2. brain tumor 3. TIA 4. Syncope case comments N1: EEG is normal- we can rule out epilepsy; if EEG is normal, it is most likely- precentral gyrus tumor/basal ganglia/spinal cord pathologies If EEG abnormal, you think about simple partial seizures Diagnostic tests: 1.electroencephalography(EEG)- tests that detects abnormalities in brain waves and electrical activity in brain 2. MRI of brain to look for lesions Treatment: 1. first line: anti-epileptic drugs(benzodiazepines) 2. prevention: anticonvulsants(phenytoin) 3. epilepsy surgery: remove the causative factor of seizures, e.g. tumor

17-year old with head injury, soccer player, unconscious for 1-2 min, but then he was fine. during hospitalization, cranial nerves were found to be normal. he could not name the city, date, symptoms included headache, photopobia, stiff neck, kerning signs positive. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: subarchnoid space(between arachnoid and pia matter) diagnosis: subarachnoid haemorrhage case comments N1: *kerning sign positive bcz of infla to the meninges caused by movement of spinal cord or nerves against the meninges *absence of fever and infectious symptoms eliminates meningitis *additional symptoms to look out for in exam; sudden acute thunderclap headache, reduced consciousness, neck stiffness, kernig differential diagnosis: 1. SAH 2. meningismus 3. brain concussion 4. intraventricular haemorrhage diagnostic tests: 1. lumbar puncture between L3-L4(presence of blood may be observed(gold standard) 2. CT with angiography treatment: SPO 1. symptomatic treatment 2. prevention of complication(vasospasm(amlodipine), hydrocephalus(shunting/drainage), decrease ICP(manitol and rebleeding) 3. open surgery

Army man, unconscious and after regaining consciousness he feels lethargic, small pox vaccine, meningial symptoms with clear CSF and increased protein, 6th CN palsy

Aseptic Meningoencephalitis

Scenario N1: 60 years old man. Weakness on the left side (involving arms, trunk, and legs). Exam: 1. ptosis, 2. paralysis of the face of the right side, 3. impaired lateral gaze on the right side. T=38, BP=150/98 Scenario N2: 62yo female, conscious but mildly confused with history of TIA. Arterial pressure is high. Face is drooping on one side of face. Half side facial palsy. Abducens palsy (nose rest position) and contralateral hemiplegia. TIA history "Babinski absent" = Negative Babinski = Normal = Plantar response 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

Damage to the base of the brainstem at the level of the pons, affecting CN VI and CNVII(presenting as Fonville's alternative syndrome) Diagnosis: Lacunar infarct of the Pontine arteries(ischemic stroke of the pontine arteries) case comments N1: Pathology: Occlusion of pontine arteries which arise from basilar artery. Damage of the base of the brainstem to the abducens and facial nerve causes peripheral palsy on the side of damage and contralateral hemiplegia. Contralateral hyperkinesia (tremor, chorea, athetosis) due to involvement of red nucleus. Contralateral rigidity(cogwheel) (substantia nigra) *The symptoms presented in the case are classic for "Foville's alternative syndrome" *peripheral facial and abducens palsy with contralateral central hemiplegia-"Foville's alternative syndrome" *peripheral palsy of facial nerve= ptosis Diferential diagnosis: 1. Lacunar infarct of the pontine arteries 2. subtentorial tumor 3. cerebelar hemorrhage 4. vascular malformation(arteriovenous malformation) 5. Myasthenia gravis 6. Bells Palsy 7. 6th CN palsy 8. Tumor in posterior fossa 9. Hemorrhage in posterior fossa 10. Vertebrobasilar artery hemorraghic stroke 11. Vertebrobasilar artery ischemic stroke Diagnostic tests: 1. Neurological exam of CN VI and CN VII 2. CT with angiography treatment: TEEL 1. thrombolytic(IV TPA- tissue plasminogen activator within 3 h) 2. Embolectomy(removal of clot within 8 h) 3. Endovascular sitenting 4. Long-term management- aspirin

• Malignant tumor of ependymal cells; usually seen in children • Most commonly arises in the 4th ventricle; may present with hydrocephalus • Perivascular pseudorosettes are a characteristic finding on biopsy. • Supratentorial thus involving the lateral ventricles • Subtentorial thus involving the 4th ventricle

Ependymoma

patient has neglect(not taking care of themselves/looks disheveled and has seizures)

LOCALIZATION-hippocampus, limbic system, Cerebral cortex and Cerrebellum, if there's ataxia or cerebellar signs DIAGNOSIS-Encephalopathy due to DRAVET SYNDROME Encephalopathy is the Disruption or alteration of normal brain function or Brain structure) *case comments N1: CAUSE-SCN1A Mutation that codes for NAV1.1 protein which is a componnt of sodium Channels(+NA) Symptoms-Seizure (onset of febrile seizures-could be tonic or clonic),seen in small children Adults have secondary generalized or focal seizure, decline in mental function and they don't take care of themselves so there's signs of neglect Differential diagnosis: 1. Epilepsy 2. Tick borne encephalitis (seizure of Krozhenikhov, myoclonic) 3. Brain abscess (due to infection) 4. SSPE-Subacute sclerosing panencephalitis(cz there's signs of mental regression) Diagnostic tests: 1. EEG, 2. Gentic testing, 3. MRI to rule out mass and you'll see cerebral or cerebellar atrophy 4. Lumbar puncture to rule out encephalitis Treatment: Triple-therapy- 1. Valproate-anti epileptic, 2. styropentil-barbiturates to abort the seizures 3. clopezambenzodiazepine 4. Give phenfloramine and make sure they have ketogenic diet Prognosis -unfavorable It's very resistant to treatment so children almost always dies. case comments N2: Complication-Sudden unexpected death in Epilepsy,Patients randomly die without prior illness so if a patient randomly dies and the have epilepsy it might be due to dravet.

Motor findings - Deficits usually affect both legs but are often asymmetric Sensory findings - Weakness in lower extremities, paraesthesia, gait difficulty Sphincter disturbance - Bladder and rectal sphincter paralysis usually reflect involvement of S3-S5 nerve roots Intense local back pain is felt at first (root pain), meningeal symptoms, followed within hours or days by neurological signs of spinal cord involvement.

Localisation: Depends on where the symptoms appear Diagnosis: Spinal Cord Compression case comments N1: *Pathology: Mechanical compression of spinal cord *Spinal epidural hematoma arises spontaneously, as a complication of trauma. *in the case of compression of the spinal cords occur paraesthesia, conductive disorders of sensitivity and mild paresis of extremities below the injured area with the impairment of pelvic organs function. case comments N2: *Causes: Herniated disc Bone fragment Spinal epidural haematoma Differential Diagnosis: Extramedullary tumour Spinal cord concussion/contusion Transverse myelitis Diagnostic Tests: CT, MRI or X-ray of spinal cord Prognosis and Treatment: Surgery to relieve pressure on spinal cord by treating underlying cause

Scenario N1: 50 y/o woman, irregular movements of hands & legs, increased tone of limbs, dystonia (torsion dystonia) used to forget daily work, slow thinking, speech issues. Scenario N2: 46 y/o man, deteriorative cognitive function, started to do think slowly, speech problems, personality changes, fidgeting at night, memory loss

Localisation: Neurodegeneration of GABAnergic neurons in (sub thalamic nucleus, caudate and putamen in basal ganglia) Diagnosis-Huntington's disease Differential Diagnosis: Parkinson's disease Alzheimer's disease Wilson's disease Lewy body disease Sydenham's Chorea - Chorea of Rheumatic origin, mainly observed in Children and has a favourable outcome. Diagnostic Tests: Genetic testing (>36 CAG trinucleotide repeat)gold standard MRI- you'll see degeneration of caudate and putamen nuclei Prognosis-Poor prognosis. Patient's usually die 10-20 years after onset of symptoms either due to aspiration pneumonia or suicide. Treatment: NO CURE There is no cure for this disease as it is a progressive neurodegenerative disease. Best thing to do is treat the symptoms. Neuroleptics (Dopamine receptor antagonists), Tetrabenazine may help with involuntary movements (depletes Dopamine, for treating Chorea) 1. Physical Therapy 2. Dopamine Inhibitors *case comments: Pathology: Autosomal dominant inheritance. Repeating sequence of CAG in DNA is increased in chromosome 4, HTT gene (normal is 10-35. In Huntington disease, it is >36). Mutated proteins aggregate within the neuronal cells within the caudate and putamen which cause neuronal cell death. Tissue loss of affected areas leading to expansion of lateral ventricles. Decreased GABA, decreased Ach, increased Dopamine. Epidemiology: Onset 40 years, affects both sexes. Progressive deterioration/CNS involvement. Symptoms: Signs: Hyperkinesia or involuntary movements which can involve: Chorea - Short lasting involuntary movement that affect multiple group of muscles "looks like a dance"- purposeless dance like, jerky movements. Athetosis - Slow snake-like movements. Limbs are rotating around axis (torsion dystonia) These movements cannot be suppressed by the patient, stops with sleep. Neuropsychiatric disease - Dementia, personality changes and depression. Abnormal eye movements, Poor coordination.

60 yr old woman, went to a general physician for high fever, the doctor advised her to get a consult and admit her to the hospital but she didn't do that, after a few months she got a tonic-clonic seizure and fell into a coma. After 2-3 days/ not sure of days) she recovered from a coma. She moved to a new place and felt better and got consult/ admission in NEW VISION hospital. Neurological exam results: Lower limb paralyzed and cannot walk, upper can't take objects and move. She was not ataxic but confused. She had difficulty with communication.

Localisation: Panencephalitis therefore affects both the grey and white matter of the brain parenchyma (bodies of neurones) Inferior frontal and temporal lobes Diagnosis -Viral (HSV) Encephalitis case comments N1: Pathology: Infection of brain parenchyma Symptoms: General symptoms - headache and fever. Evolves to seizures and impaired consciousness over several days (Inferior frontal and temporal lobes are selectively involved), olfactory, or gustatory hallucinations, behavioural disturbance, complex partial seizures, dysphagia (dominant hemisphere) and hemiparesis. There's gustatory hallucination. Cerebral oedema may result in tentorial herniation Differential Diagnosis: Subacute sclerosing panencephalitis(they're both polio encephalitis) Lethargic encephalitis Tick borne encephalitis Diagnostic Tests: Brain MRI-hyperdensities of frontal and temporal lobes Lumbar puncture Prognosis and Treatment: favourable if treated. Bed rest, fluids and anti-inflammatory drugs such as ibuprofen and paracetamol for headache and fever relief. Acyclovir 3000 mg/day (in acute stages) in AM for 5-7 days, then oral administration for 7-10 days *case comments N2: Subacute sclerosing Panencephalitis(SSPE) Localization-Grey and white matter of the brain(brainstem,cerebellum,spinal cord) SSPE is caused by measles; and less common worldwide due to vaccination. Changes involve both white and grey matter, especially in the posterior hemisphere; brainstem, cerebellum and spinal cord are also affected. Marked gliosis occurs with perivascular lymphocyte and plasma cell cuffing; oligodendrocytes contain eosinophils inclusion bodies. Clinical duration and features • Stage I: behavioral problem, declining school performance; progression dementia • Stage II: chorioretinitis, myoclonic jerks, seizures, ataxia, and dystonia • Stage III: lapse into rigid comatose state Subacute sclerosing panencephalitis (Dawson's disease) due to reactivation of measles virus or inappropriate response to measles virus 2-10 years after original viral attack

symptoms that disease started with: fever, malaise, sore throat, afterwards added: headache, photophobia, drowsiness during exam found: Mild meningism, Neck stiffness, Kernigs positive, Skin rashes, Parotitis Diarrhoea, Myalgia

Localisation: infection and Inflammation of the leptomeninges (arachnoid mater and pia mater) of brain spinal cord and CSF Diagnosis: Meningitis - Viral/(aseptic meningitis) case comments N1: Pathology: This is a viral serous secondary meningitis. Most commonly caused by enteroviruses (coxsackievirus A, coxsackievirus B and echoviruses). Causes: Enteroviruses - coxsackievirus A, coxsackievirus B and echoviruses. Other viruses - herpes virus, measles, mumps, varicella virus and flaviviruses such as West Nile virus and HIV. Symptoms: Stage 1 (prodromal): fever, malaise, sore throat Stage 2 (meningeal phase): headache, photophobia, drowsiness Stage 3 (recovery) after 7-14 days Complications include Febrile seizures, inappropriate ADH secretion Differential Diagnosis: bacterial meningitis ADEM after infections Diagnostic Tests: Lumbar puncture - Clear, normal/slightly increased PMN cells, markedly increased lymphocytes, normal/slightly increased protein, normal glucose PCR to detect virus. Prognosis and Treatment: Good prognosis, most recover without medication some may require anti-viral medication such as acyclovir (HSV)

*Myotonia (a tonic spasm of muscle after voluntary contraction) (exacerbated by cold and most pronounced after period of inactivity) *Muscular hypertrophy and hyperexcitability (Athletic habitus) Signs *Grip myotonia (inability to release handshake) is characteristic At first, patient cannot carry out rapid movements but can after repeated attempt *Hypertrophic masseter muscle Percussion myotonia: Myotonia can be induced be tapping the muscle belly, which results in spasmatic muscle contraction. Also occurs when tongue is tapped with neuro hammer.

Localisation: voltage dependent Cl- channel gene of skeletal muscles Diagnosis: Myotonic Dystrophy (Myotonia Congenital Thomsen's disease) Case comments N1: Pathology: Progressive loss of skeletal muscle due to autosomal dominant inheritance Epidemiology: Manifests at an early age and can manifest during the 1st or 2nd decade of life. Differential Diagnosis: Duchenne's MD Becker's MD Landouzy-Dejerine Facioscapulohumeral Muscular Dystrophy Erb-limb girdle MD Diagnostic Tests: EMG - Low amplitude, high frequency potentials continue for many seconds after end of voluntary contraction, Muscle biopsy- reveals no abnormality other than enlargement of muscle fibers, and this change occurs only in hypertrophied muscles. Prognosis and Treatment: Good prognosis (Normal life expectancy). Less severe over time. Local anaesthetics and anticonvulsant such as mexiletine to decrease myotonic rigidity, anti-arrhythmics, Baclofen, Acetazolamide (palliative effect on Thomsen's form of myotonia congenital)

*Atrophy in shoulder spreads to pelvic region or vice versa *Limb-girdle weakness *Proximal muscle involvement > distal muscle *Waddling gait - due to the weakness of pelvic muscles and not ataxia. *Gower's sign *Lordotic posture *Pain is not typical. *No somatosensory disturbances * Normal mental function.

Localization-Shoulder girdle and pelvic girdle muscles Diagnosis: ERB LIMB GIRDLE MUSCULAR DISTROPHY case comments N1: *Pain, if present, is due to impaired muscle metabolism and not nerve involvement. *Pseudohypertrophy may occur *Cardiac involvement rare case comments N2: Pathology: Autosomal recessively inherited disorder. Classified into LGMD 1 (AD)-6 forms and LGMD2 (AR)- this is more common and has 11 forms. Limb girdle weakness without weakness of facial muscles and hypertrophy. Differential Diagnosis: Becker's MD Duchenne's MD Landouzy-Dejerine Facioscapulohumeral Muscular Dystrophy Spinal muscle atrophy Poliomyelitis Diagnostic Tests: Genetic testing Blood tests - Increased CK EMG Muscle biopsy Prognosis and Treatment: No cure but Steroids (prednisone) can be used to slow down muscle damage

Patient with damage to CN7 and CN10 and was drunk. Common symptoms include: confusion(about time, place and person), memory loss, poor balance and gait(ataxia) 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

Localization: 1. Limbic system 2. Hypothalamus 3. Thalamus 4. Cerebellum 5. Brainstem Diagnosis: Wernicke's encephalopathy(*Classic triad symptoms of Wernicke's encephalopathy: confusion, ataxia, nystagmus) Differential diagnosis: 1. Wernicke's encephalopathy 2. Wernicke's Korsakoff syndrome(WKS, only if there are confabulations, anterograde amnesia, retrograde amnesia) 3. vascular dementia 4. Alzheimer's 5. Brain tumor Diagnostic tests: 1. blood and liver function tests(to check for thiamine levels: 2.5-7.5 μg/dL) 2. CT or MRI(to check for degeneration of mamillary bodies) Treatment 1. IV thiamine infusion(250-300 mg thiamine 2 timex a day for 3-5 days) 2. Give glucose but must make sure that the thiamine levels are normal

Scenario N1: A 58-year-old man with liable HTN. In the usual state of health up until this morning when he noted the onset of severe vertigo, with spinning on the left along with an 8/10 occipital headache. He vomited twice and his wife noted that he was having more difficulty controlling his right hand, knocking his coffee cup to the floor. she called an ambulance and by the time they arrived, he was lying on the kitchen floor, awake but confused and agitated. his BP was 185/110 and he had tachycardia, sweating profusely as well as intermittent retching. he continued to complain of the headache and was transported to the ED. Scenario N2: Hypertension, nystagmus, vertigo, sensation intact but all extremities have hyperreflexia(cerebellum+UMN). the wife said he was unable to hold a coffee mug. when the ambulance came he was found lying on the floor conscious but confused. Exam: In ED he was awake and agitated with PB 190/120 in both arms and was tachycardia at 105. His attention waxed and warned but he complained of nausea and vertigo with most prominent feelings of rotten and pitching to the left. Nystagmus was most evident when looked to the left but there was a significant up and downbeat nystagmus as well as some clockwise rotary component and reactive. there was no nuchal rigidity. he denied any sensory asymmetry. he had good strength in all limbs. his reflexes were brisk but symmetrical in all limbs and there was no clonus. his toes were downing. he was unable to walk. Scenario N3: 52 year old, previous respiratory infection, HTN, Can't hold jug, symmetric hemiparesis from lower limb 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

Localization: Basal-ganglia, cerebellum, Pons Diagnosis: intracerebral hemorrhage(hemorrhagic bcz high BP and signs of high ICP) in the posterior fossa Differential diagnosis: 1. Anterior Inferior Cerebellar Artery(AICA) hemorrhagic stroke 2. Anterior Inferior Cerebellar Artery(AICA) ischemic stroke 3. Intracerebral hemorrhage in the posterior fossa 4. Cerebral tumor of posterior fossa Lab Diagnostic Tests: MRI for hemorrhagic CT with 12 slices to check for blood or ischemia Treatment: -Acute management-decrease blood pressure to less than 160, Avoid complications Surgical exploration and clipping or repair of damaged artery if blood volume is more than 50ml to avoid complications like herniations, etc. CPL 1. Clipping(surgical prevention of further bleeding) 2. Painkillers 3. Long-Term management- Antihypertensive Medication(CCB) Additional hints: the main symptoms we have are: 1. nystagmus, which indicates damage in the midbrain or pons(CN3/4/6) 2. hyperreflexia of extremities: which indicates central UMN palsy 3. vertigo: which indicates damage in the pons(CN VIII) 4. occipital headache(migraine) 5. confused, agitated but conscious 6. hypertension/tachycardia: center for regulation is located in the pons/medulla 7. walking(gait) problem which indicate cerebellum *the common location affected above is the PONS- supplied by ICA(AICA)

Hypertension, nystagmus, vertigo, increased BP, sensation intact but all extremities have hyperreflexia. Wife said he was unable to hold a coffee mug, when ambulance came, he was found lying on the floor conscious but confused. Additional info found about this case A 58 y/o man with liable HTN was in is usual state of health up until this morning when he noted the onset of severe vertigo, with spinning on the L along with an 8/10 occipital headache. He vomited twice & his wife noted that he was having more difficulty controlling his R hand, knocking his to the floor. She called the ambulance & by the time they had arrived he was lying , awake but obviously confused & agitated. His BP was 185/110 & he was tachycardia, sweating profusely as well as intermittently retching. He continued to complain of the headache & was transported to the ED. Examination: In ED he was awake & agitated with BP 190/120 in both arms & was tachycardia at 105. His attention waxed & warned but he complained of nausea & vertigo with most prominent ●feelings of rotten & pitching to the L. Nystagmus was most evident when looked to the L but there was a significant up & downbeat nystagmus as well as some clockwise rotary component & reactive there was no nuchal rigidity. He denied any sensory asymmetry. He had good strength in all limbs. His reflexes were brisk but symmetrical in all limbs & there was no clonus. His toes were downing. He was unable to walk. There was no nuchal rigidity

Localization: Cerebellum and midbrain Diagnosis: Superior Cerebellar Artery (SCA) stroke, that artery supplies: 1. Superior cerebellum and 2. Posterolateral midbrain Vestibulocochlear affected causing gait Differential diagnosis: 1. Superior Cerebellar Artery (SCA) ischemic stroke 2. Superior Cerebellar Artery (SCA) haemorrhagic stroke 3. Intracerebral haemorrhage in posterior fossa 4. Cerebral tumour of posterior fossa case comments N1: *In hypertensive patients, hemorrhage more common than ischemic stroke *Rupture of branches of SCA causes cerebellar hemorrhage. Characteristics of this include severe occipital headache, dysarthria, N/V, vertigo, unsteady gait, head turning and gaze deviation to the side opposite the lesion. diagnostic tests: MRI for hemorrhagic CT with 12 slices to check for blood CT scan with angiography for ischemic Prognosis and Treatment: Acute management then surgical exploration and clipping case comments N2: *SCA stroke symptoms: Cerebellar signs - disturbed gait, limb ataxia, incoordination of limbs (they are laging). Brainstem signs Ipsilateral Horner's syndrome Ipsilateral sensory loss of face (pain and temperature - LST) Contralateral body pain and temperature loss - cerebral conductive syringomyelic dissociation

Babinski reflex comes and goes, ankle reflex absent, meningeal symptoms present, infection, leg rigidity billaterally, absent abdominal reflex, achilles sometimes comes and goes and loss of deep sensation in lower abdomen. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

Localization: Spinal cord segments at the level of T6-T12, due to inflammation(integrated centre of the abdominal reflex is at the level of this as well as all the other reflexes below will be damaged too). discuss the case: Loss of deep sensation in the lower abdomen means bulbothalamic tract damage(deep sensation). Diagnosis: Transverse myelitis *infection(causes meningeal symptoms) *damage to corticospinal tract(below lesion leg rigidity) *abdominal reflex starts at t8 level so lost below lesion loss of deep sensation(below lesion damage to bulbothalamic) Differential diagnosis: 1. Transverse myelitis 2. Multiple Sclerosis 3. Intramedullary tumour 4. Extramedullary tumour 5. transverse dissection of spinal cord 6. ADEM 7. spinal cord compression Diagnostic tests: 1. lumbar puncture(increase in protein and increase in IgG)- to rule out meningitis 2. MRI Treatment: 1. Corticosteroids(supresses inflamation) 2. Antibiotics(if bacterial- penicilin G) or antiviral to treat infection and IV IgGs and plasma paresis(to eliminate autoimmune antibodies) methylprednisone, IgG Transverse myelitis- across the spinal cord, inflamation of myelin physiotherapy, occupational therapy

Head injury while playing soccer with elbow of another player, unconscious for several mins then was normal. After 6 hours had confusion, headache, disorientation and again orientated after several minutes. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

Localization: brain parenchyma and reticulus formation Diagnosis: Brain concussion *symptoms indicate nonmorphological damage to the brfain parenchyma case comments N1: no loss of conscousness- no concussion Differential diagnosis: 1. frontal lobe concussion 2. frontal lobe contusion 3. epidural hematoma 4. subarachnoid hematoma case comments N2: *contusion affects specific part of brain *you can't localize specific lobe without no mentioning in history(e.g. frontal lobe concussion or etc.), that's why diagnosis is brain concussion, not frontal lobe concussion Diagnostic tests: 1. craniography, to rule out fractures, 2. CT or MRI(to see if there are additional cerebral damages) 3. ophtalmoscopy, 4. CSF analysis Treatment: 1. painkillers 2. bed rest 3. hydration case comments N3: 1)Concussion: reversible traumatic affection without morphological lesions(no damage of brain parenchyma). clinical signs and symptoms: brief transient loss of consciousness no more than 1-20 minutes followed by period of confusion, you may also have transient amnesia(loss of memory) -absence or decreased corneal reflex -anesocoria- more than one mm of difference in diameter of pupil -nistagmus -palmar chin reflex -unsteady gait diagnosis: craniography, ophtalmoscopy, CSF analisis treatment: transient restriction of activity(bedrest 7-10 days), hydration, antioxidants(vit C), analgesice complication: post-concusion syndrome, which is characterized by chronic headache and depression 2)brain contusion: injury which involve the brain parenchyma clinical manifestations: cerebral system(headache, vomiting), meningeal symptoms plus possible focal symptoms, fracture, subarachnoid bleeding, longer period of unconciousness diagnosis: craniography, ophtalmoscopy, csf analysis, CT/MRI(in order to assess focal damage or pare injury) treatment: observation, maintenance of vital signs, decrease ICP, new therapeutic hypothermia(to decrease body T 34 degrees) 3)brain compression: caused by subdural, epidural and intracerebral haematomas clinical symptoms: increased cerebral symptoms(headache/vomiting, dizziness) presence of focal and brainstem dislocation symptoms, "lucid space period"- you feel quite well and then rapidly feel worse diagnosis: craniography, ophtalmoscopy, csf analysis, CT/MRI

24 year old boy. Part of the team. no sensory or motor deficit. only ataxic gait. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

Localization: damage to the cerebellum Diagnosis: subtentorial tumor or cerebellar stroke *walks in zigzag like drunk man, sway side to side(due to damage to vermis) Differential diagnosis: 1. Subtentorial tumor 2. brain concussion 3. Brain contusion 4. brain compression Diagnostic tests: 1. Neurological examination 2. Cerebellar Examination 3. Blood tests(to define underlying causes: stroke, tumor, infection) 4. MRI/CT Treatment: dependent on the cause 1. Treat underlying cause(e.g. tumor) 2. treat symptoms 3. therapies: physical, occupational, and speech therapy *why it is not cerebral ataxia? -bcz no motor, no sensory deficit *can't have "cerebellar ataxia" as a clinical diagnosis as it is a symptom due to an underlying disease

Scenario 1: 51-year old woman is brought by ambulance to ED where multiple injuries are being evaluated including rib fractures, pelvic fractures and possible splenic injury. She is awake, although sedated due to severe back and shest pain bilaterally. the nurse states, that she is not moving her legs. She has a bladder catheter in place and urine is clear. Histroy is remarkable. exam: according to multiple trauma neurological exam is difficult. Upper limb movement seems good, but she is not moving her legs. Sensation is patchy in lower extremities and in the trunk with apparently normal sensation in the chest and back above the T9 dermatome. Superficial upper(superior) abdominal reflexes bilaterally are absent. reflexes and strength in the arms are normal, but reflexes in the legs are absent, as no plantar response. Scenario 2: 54-year old woman brought to ED. Injuries including rib fractures, pelvic fractures and splenic injury. She is awake, although sedated due to severe back and shest pain bilaterally. no leg movements, bladder catheter in place. upper limbs are good. sensation in chest and back is normal(above T9). Abdominal reflex absent. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

Localization: spinal cord segments at level of T6-T8 Diagnosis: Spinal cord compression at level T6-T8 *damage to corticospinal tract below lesion-loss of leg movements *damage to anterior horns- abdominal reflex starts at level of T6(so below lesion is absent) *damage post ganglionic sympathetic innervation impairs urine and fecal continence case comments N1: in general: when we have dermatome number i.e. T9 deficit in motor tract should be below or a level. but in case of deficit in sensory tract should be 2-3 segments above the segment affected: so here will be T7 differential diagnosis: 1. spinal cord trauma/compression 2. spinal cord contusion 3. spinal cord concussion 4. spinal cord tumor case comments N2: view into on previous page regarding abdominal reflex; Superficial reflex has integrated centre at T6-T8 so therefore spinal cord damage at level T6-T8; Since the bladder receive sympathetic innervation, the integrated centres of this system are located in thoracolumbar segments: hence for this reason you can understand the damage of the integrated centre causes bladder incontinence; the synonym of sympathetic is colinergic and thoracolumbar; parasympathetic synonim is adrenergic, craniosacral Diagnostic tests: 1. Neurological exam to determine level of lesion 2. X-ray 3. CT or MRI Treatment: 1. immobilization 2. surgical removal of bony fragments 3. pain-relief(analgesics, NSAIDS) 4. vitamin B12 5. rehabilitation case comments N3: it is recommended that physicians consider vitamin B12 deficiency in their patients with SCI, particularly, in those with neurologic and or psychiatric symptoms. These symptoms often are preventable if treatment is initiated early.

24-year-old female. pain in chest, fever, cough, wood like leg in the morning, superficial sensations lost, plantar reflex abnormal, abdominal reflex absent 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

Localization: spinal cord segments at the level of T6-T12, due to inflammation Discuss the case: fever, cough- signs of infection, wood like leg in the morning- damage of the corticospinal tract, superficial sensation loss-damage of the lateral spinothalamic tract, abdominal reflect absent- damage at the level of T6-T12 Diagnosis: Transverse myelitis *infection- fever, cough *damage of the corticospinal tract, below lesion-wood like leg in the morning *abdominal reflex starts at T8 level so lost below lesion *damage of the lateral spinothalamic tract-superficial sensation loss below the lesion Differential diagnosis: 1. Transverse myelitis 2. Multiple Sclerosis 3. Intramedullary tumour(ADEM) 4. Extramedullary tumour(spinal cord compression) 5. transverse dissection of spinal cord Diagnostic tests: 1. lumbar puncture(increase in protein and increase in IgG)- to rule out meningitis 2. MRI Treatment: 1. Corticosteroids(supresses inflamation) 2. Antibiotics(if bacterial- penicilin G) or antiviral to treat infection and IV IgGs and plasma paresis(to eliminate autoimmune antibodies) methylprednisone, IgG Transverse myelitis- across the spinal cord, inflamation of myelin physiotherapy, occupational therapy

26 year old women, upper limb superficial sensation loss. While doing things, she burnt her own left hand and never felt a thing clumsy gait, tripping, difficulty typing. Lower limb reflexes are normal. Compound sensation normal. Hyperreflexia, back pain, ataxia and headache. No meningismus symptoms. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

Localization: syrinx cavity in the central canal of spinal cord at the level of C5-C8 case comments N1: *localization is C5-C8 not T1 bcz there are no repiratory problems. *if there are respiratory problems you will also mention T1 and T2 bcz brachial plexus is from C5-T2 diagnosis: syringomyelia case comments N2: *fromation of syrinx in the centre of spinal canal in the spinal cord *affects both anterior spinothalamic and lateral spinothalamic tract *spinal conductive(?) syringomyelia *bilateral superficial sensory loss of upper extremities(cape like distribution) differential diagnosis: SHID 1. Syringomyelia 2. Hematomyelia 3. Intramedullary tumor 4. disc herniation case domments N3: *signs and symptoms of syringo myelia, which might affect your back, shoulders, arms or legs, can include: muscle weakness and wasting(atrophy) loss of reflexes loss of sensitivity to pain and T headaches stiffness in your back, shoulders, arms and legs pain in your neck, arms and back spinal curvature(scoliosis) diagnostic tests: 1. exam of superficial sensation 2. MRI of the spinal cord(syrinx cavities) treatment: depends on specific cause: 1) if arnold chiari malformation type 2- posterior fossa decompression surgery 2) if hydrocephalus- syrinx drainage of CSF via shunt case comments N4(from Osmosis): syringomyelia features: -chronic, onset 10-35 year old -formation of cavities of syrinx in central canal of the spinal cord(cervical C5-C8 brachial plexus) -associated with arnold chiari malformation -hypoplasia/posterior cranial fossa and tonsils of cerebellum descend below foramen magnum symptoms: symmetrical loss of superficial sensation in both upper limbs as known as "jacket like phenomenon" complications: syringobulbia- due to cavity formation in medulla CN9 and CN12 are affected cardiovascular and respiratory problems case comments N5: syringomyelia is a disorder in which a fluid-filled cyst (called syrinx) forms within the spinal cord. Over time, the syrinx can get bigger and can damage the spinal cord and compress and injure the nerve fibers that carry information to the brain to the rest of the body. syringomyelia, the watery liquid known as CSF-which normally surrounds and protects the brain and spinal cord- builds up within the tissue of the spinal cord, expands the central canal and forms a syrinx. Generally, a syrinx develops when the normal flow of CSD around the spinal cord or lower brain stem is disturbed, when syrinx affect the brain stem, the condition is called syringobulbia. syringobulbia is a medical condition in which syrinx, or fluid-filled cavities, affect the brainstem(usually lower brainstem) syringobulbia usually causes pain. it may also cause a loss of sense of T. alveolar hypoventilation(insufficient breathing, a type of central hypoventilation syndrome) may occur, with hypercapnia(excess blood CO2), stridor(an unusual breathing sound) and irregular breathing case comments N6: *syringomyelia: syrinx-"cyst", "cavity", myelia- spinal cord, cystic enlargement of spinal cord. *starts medially, expands out, damages spinothalamic tract patho and causes: *CSF cyst around spinal cords central canal *cyst in nerve tissue(syrinx), spinal cord(myelia)=e.g. brainstem syrinx(syringobulbia) *as cyst forms, grows-fluid collects within spinal cord tissue-increase pressure within spinal cord-damage *symptoms progress slowly, often adult diagnosis Risk factros *congenital: arnold-chiari malformation, genetic mutation *aquired: trauma, spinal cord tumor, bleeding, scoliosis signs and symptoms *various locations, syringomyelia severity *chronic pain, dysesthesia, paresis/paralysis *suspended sensory level *sensory perception defect only on body parts innervated by syringomyelia-affected structures diagnosis MRI(syrinx visualization in spine neurological exam(for suspended sensory level) treatment surgery(cyst drainage, flow restoration

That tumor may present as intrasellar secretory or non-secretory masses • Acidophilic adenoma: overproduces growth hormone, leading to gigantism prior to puberty or acromegaly after puberty • Basophilic adenoma: produces ACTH, leading to Cushing syndrome • Chromophobe adenomas: are responsible for most of the endocrinopathies caused by pituitary tumors • Many secretory tumors are microadenomas, found only after endocrine abnormality is discovered; the most common endocrine hypersecretion is prolactin, producing amenorrhea and gynecomastia in men.

Pituitary adenoma

50 year-old patient, slowly progressive course, with arm weakness, dysphagia(solids/liquids), some flaccid/spastic muscles, no sensory symptoms 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

case comments N1: *arm weakness- upper limbs more involved *solid/liquid dysphagia-bulbar palsy localization: localization of patho process: coticospinal tract(UMN and anterior horn)(LMN and corticobulbar tract) 1. 5th pyramidal cells of precentral gyrus 2. anterior horns of spinal cord 3. pyramidal tracts(corticospinal tract in the lateral columns) 4. motor neurons of medulla diagnosis: amyotrophic lateral sclerosis/Lou Gehrig's disease UMN: spastic paralysis of muscles(clasp-knife reaction) LMN: flaccid paralysis of muscles differential diagnosis: 1. ALS 2. multiple sclerosis 3. myasthenia gravis 4. guillain barre syndrome 5. bulbar palsy lab diagnostic tests: 1. electromyography(to assess nerve conduction in UMN and LMN activity) 2. MRI 3. nerve conduction related studies treatments: no cure *riluzole(supresses glutamate toxicity) *baclofen- reduces muscle spasticity *amitriptyline(tricyclic antidepresant) *supportive care: pain reliev=f, bed rest case comments N2: *amyotrophic= progressive wasting and weakening of muscle tissue *lateral= involvement of lateral column *sclerosis= scar formation andreplacement of degenerated and lost motor neurons by glial cells case comments N3: clinical presentations: -progressive assymetric weakness starting from upper limb -fasciculation, muscle cramping and atrophy -hyperreflexia, stiffness, clumsiness above are all limbs related case comments N4: *bulbar related as known as medulla related: hoarseness, dysarthria, dysphagia, tongue fasciculation, dysphonia, emotional liability(pesudobulbar palsy)

29-year old woman with twins presents to the emergency with 2-hour history of ptosis, headache and miosis(no pupil dilation). she complains of unsteady gait and how she keeps falling. she also complained that when she tried picking up her phone to call the ambulance, her hands kept shaking and was unsteady. she also has loss of pain and T in the right hand, right side of trunk and right leg 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

case comments N1: *ptosis- CN3 involvement *headache, miosis without vomiting- maybe hemorrhage excluded *unsteady gait- cerebellum *hands kept shaking- intention tremor *loss of pain and T- loss of superficial sensation(spinothalamic tract) localization: left superior cerebellum and midbrain diagnosis: superior cerebrellar artery(SCA) ischemic stroke on the left side *oculomotor deficit= ptosis and miosis *infarct of the cerebellum(superior cerebellar peduncle)= gait and intention tremor *infarct of tegmentum(part of midbrain)= spinothalamic tract(loss of superficial sensation)- pain and T differential diagnosis: 1. Superior cerebellar artery (SCA) ischemic stroke 2. Superior cerebellar artery (SCA) hemorrhagic stroke 3. intracerebral hemorrhage in posterior fossa 4. cerebral tumor of posterior fosaa diagnostic tests: 1. MRI 2. CT scan with angiography treatment: TEEL 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin case comments N2: problem= gait, shaking of hands= cerebellum ptosis, miosis= CN 3

50 year old male, sensory deficits, hypertension, vertigo, vomiting, severe headache, loss of consciousness, can't remember anything, confused, extremities, upper limbs are fine. Lower limb paralyzed 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

case comments N1: *vomiting, severe headache, loss of consciousneess- signs of hemorrhage *lower limb paralysis- upper precentral gyrus involvement localization: upper part of precentral gyrus(frontal lobe) diagnosis: anterior cerebral artery(ACA) hemorrhagic stroke(intracerebral) case comments N2: *hemorrage(headache, vertigo, vomiting and increased ICP) *precentral gyrus: central palsy of lower limbs(given that upper part of precentral gyrus is damaged) on the opposite side of the lesion *postcentral gyrus: cerebral cortical dissociation with loss of compound sensation and kinesthetic sense *damage to prefrontal cortex: memory loss differential diagnosis: 1. ACA hemorrhagic stoke 2. ACA ischemic stroke 3. intracerebral hemorrhage 4. subarachnoid hemorrhage 5. frontal lobe tumor 6. brain concussion(refers to more widespread brain trauma from a blow to the head or swift shaking) *in brain concussion: memory loss is transient lasting few minutes no more than 20 minutes) 7. brain contusion(as known as bruise and bleeding on the brain due to localized trauma) lab diagnostic tests: noncontrast CT treatment: CPL 1. Clipping(surgical prevention of further bleeding) 2. Pain killers 3. Long term management- antihypertensive medication(calcium channel blockers) case comments N2: diagnosis- cerebral hemorrhagic stroke(due to the hemorrhage of the ACA) 2 mechanisms of hemorrhage: 1. per rhexis- by rupture so the blood vessel ruptures and that's the cause of hemorrhage 2. per diapedesum- there is increased permeability of the wall of the vessels and so blood seeps out and inhibits the brain tissue

45 year old male, car accident, conscious but sedated, due to severe back ache, he shows both sensory and patho weakness of left upper limb along with loss of tendon reflex, central palsy in left lower limb. on opposite side loss of pain, T and tactile. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

case comments N1: 1. sensory and patho weakness of left upper limb- lateral spinothalamic tract(lateral column, same side same level) 2. loss of tendon reflex- peripheral palsy(same side same level) 3. central palsy in left lower limb(corticonuclear tract(lateral columns, same side below the level) opposite side looss of pain, T and tactile- lateral spinothalamic tract(laterla column, opposite side, below the level) localization: hemi-section of spinal cord at the level of C5-C6, on the left side(presenting as brown-sequard syndrome) case comments N2: *hemisection of half of the spinal cord involving- anterior horn, posterior horn and lateral column(affecting corticospinal tract and spinothalamic tract) Diagnosis: spinal cord compression due to trauma, on the left side case comments N3: *presenting as brown-sequard syndrome *sensory and patho weakness and loss of tendon reflex in upper limb, damage to anterior horns presenting as peripheral palsy *on the same side-sensory loss in upper limb(damage to bulbothalamic tract), central palsy(?) of the lower limb(damage to the corticospinal tract) *on opposite side loss of the pain, T and tactile- spinothalamic tract case comments N4: *weakness of left upper limb with loss of tendon reflex means: peripheral palsy is on the same side and same level *regarding central palsy in left lower limb means-is on same side and level below *regarding the opposite side of pain and T means-on the opposite side and below the level differential diagnosis: 1. spinal cord trauma/compression 2. spinal cord contusion 3. spinal cord concussion 4. spinal cord tumor case comments N5: *don't say transverse myelitis or transverse dissection of spinal cord lab diagnostic tests: 1. X-ray 2. CT or MRI case comments N6: according to this case, the brachial plexus is affected which is from C5-T2 on the same side. why the localization is C5-C6 bcz 1) according to motor manifestation they should be on the level or below the level of the damage. 2) according to somatosensory manifestation in particular, spinothalamic, the manifestation are 2-3 segments below. we are not taking account T1-T1 bcz the phrenic nerve is noit affected bcz we don't have respiratory problems. *we now narrowed down from C5-C8 and then if you go up C8 2-3 segments the localisation will be C5-C6 Treatment: ISPVR 1. immobilization 2. surgical removal of bony fragments 3. pain-relief(analgesics, NSAIDS) 4. Vitamin b12 5. rehabilitation case comments N7: what are the clinical manifestations of brown-sequard syndrome: 1. same level same side: -spinal segmental syringomyeliac dissociation(damage of posterior horn) -peripheral palsy(damage to the anterior horn) 2. same side but level below: -spinal conductive tabetic dissociation(damage of posterior column of bulbothalamic tract) -central palsy(damage of lateral column of corticospinal tract) 3. opposite side and below: -spinal conductive syringomyelic dissociation(damage of lateral column of spinothalamic)

meningeal symptoms: headache, vomiting, general hyperesthesia(increased sensitivity of any of your senses e.g. sight, sound and touch), reactive pain phenomena(over reaction to pain), hemorrhagic rash(typical sign of meningococcal infection)- due to broken blood vessels, giving the appearance of a rash caused by meningococcal septicemia). muscle tonic,neck stiffness, kernig's sigh, Brudzinski sign 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

case comments N1: hemorrhagic rash- characterized by meningococcal meningitis) localization: leptomeninges(pia and arachnoid matter) in the brain and spinal cord and CSF, due to infection diagnosis: Primary purulent meningococcal meningitis- life threatening- ask for CSF paper before diagnosing) case comments N2: neurtophilic pleocytosis- purulent lymphatic pleocytosis- serous primary- purulent secondary- only serous differential diagnosis: 1. primary purulent meningococcal meningitis 2. secondary serous tuberculosis meningitis 3. viral serous meningitis(varicella zoster, herpes simplex) 4. encephalitis(viral, tick borne) *case comments N3: if CSF will be normal diagnosis will be: SAH, meningismus, meningismus due to irritation of meninges diagnostic tests: lubar puncture between L3-L4(spinal tap) 1) turbidity 2) increased CSF pressure(>180 mmH20 in supine position and >200-300 mmH20 in sitting position) via Bullit's manometer. if there is no manometer, count the drps that come out from the needle. >60.70 drops/min= increased CSF pressure 3) pleocytosis(usually of polumorphonuclear(PMN) leukocytes); WBC counts> 10 cells/mm3 4) decreased glucose concentration(<45 mg/dl) 5) increased protein concentration(>45 mg/dl) 2. check meningeal signs: Kernig, Brudzinski and nuchal rigidity treatment: 1. antibacterial therapy in 1st hours of the disease(cephalosporins 3rd generation, oral ceftriaxone 4 mg/day or IV meronem 3 mg/day) 2. osmotic diuretics to decrease ICP(mannitol)- give osmotic to all purulent meningitis 3. dexamethasone to reduce infla 4. normalization of vital signs case comments N3: IVANE CAN ASK ABOUT THE FOLLOWING: the 3 symptoms of complexes characterising meningitis to be knowns if CSF analysis is not available: 1. syndrome of infections disease(fever, fatigue, rash, myalgia, inflammatory changes in peripheral blood) 2. meningeal syndrome(headache, vomiting, seizures, agitation and neck stiffness) 3. infla changes in CSF(by lumbar puncture in L3-L4 case comments N4: complications of meningitis: 1. subdural effusion which is more common in children 3 months- 5 years associated with seizures, persistent fever, hydrocephalus 2. waterhouse-friederichen syndrome(which occurs in the 1st hours of fulminant meningitis:\ -adrenal insuficiency -disseminated intravascular coagulation(DIC) -internal organ hemorrhage case comments N5: *normal pressure of CSF 250 mmh2o *bacterial: polymorphonuclear lymphocytes and protein increased, glucose decreased *viral: lymphocytes increased, proteins increased or normal, glucose normal *fungal/TB- same as bacterial

*Sudden onset of headache *'the worst headache of their life' *nuchal rigidity, kernig sign positive *CN palsies, focal neurological deficits

case comments N1: *focal neurological deficits - depending on site *nuchal rigidity, kernig sign positive= signs of Meningeal irritation *Consciousness may be impaired Localization: Rupture of aneurysm of one of the arteries at the base of the brain - bleeding in subarachnoid space (between arachnoid mater and pia mater) - common in anterior communicating artery (ACA), (could be due to trauma too) Diagnosis: SAH Differential Diagnosis: Meningitis/encephalitis brain contusion subdural haemorrhage Epidural hematoma Diagnostic test: Lumbar puncture MRI scan of the brain Treatment: Acute treatment-manage blood pressure to be <160 and manage or avoid complications Surgical exploration and clipping, symptomatic treatment and prevention of complications (vasospasm, hydrocephalus & rebleeding)

a 12-year old boy is brought to your clinic bcz of a gait disorder. over the pas 3 years, he has had trouble keeping up with his friends at play and had been falling during team sports. his parents adopted him from Russia, where he was orphaned. he has been sent to you by way of his family doctor, who tells you that apart from mild orthopaedic problems, the boy has no significant medical history. he has been in this country for 5 years. the patient denies any other symptoms exam: exam reveals a pleasant child of normal intelligence. General exam shows mild scoliosis and pes cavus with hammer toes. there is no hepatosplenomegaly. he is mildly dysarthric. there is no aphasia. there is bilateral horizontal nystagmus. motor exam seems normal. but sensory exam shows absent vibration and proprioception in the lower extremities with a positive Romberg sign. cerebellar exam shows hin to be ataxic, more in the legs than the arms. Deep tendor reflex(DTR) are absent, and he has bilateral Babinski sign. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

case comments N1: *gait disorder- damage of the spinocerebellar gtract(lateral columns) *absent vibration and proprioception- bulbothalamic tract-posterior columns *areflexia would be seen in Friedreich ataxia *age is before 25(10-15 years old) localization: 1. posterior column(bulbothalamic tract- deep sensation) 2. lateral column(anterior/posterior spinocerebellar tract and lateral corticospinal tract-voluntary movements, lateral column) *caused due to genetic mutation of FXN gene, leading to GAA trinucleotide repeat of more than 120 times on chromosome 9, affecting frataxin diagnosis: hereditary freidrich's ataxia -mainly affects younger population, before age 25: most commonly 10-15 year old, it's autosomal recessive -damage to bulbothalamic= loss of deep sensation -damage to spinocerebellar tract= gait ataxia(loss of unconscious proprioception) -slurred speech and dysarthria(5 years after onset) -nonneurological: pes cavus, scoliosis case comments N1: the diagnosis is dependent on following criteria: 1. progressive ataxia with an onset before the age of 25 years 2. lower limb areflexia 3. decrease of proprioceptive or vibration sense in lower limbs 4. dysarthria within 5 years after onset of ataxia differential diagnosis: 1. friedrich's ataxia 2. pierre-marie ataxia 3. charcot marine tooth disease 4. duschenn muscular atrophy case comments N2: *he wants to write down: pierre-marie disease(autosomal dominant, age of onset 30; charcot marine tooth disease(autosomal dominant: onset during 1st 10 years of life, CMTD1 and CMTD2 mutations); duschen: X-linked recessive pattern; defect of the dystrophin protein, only affects MALE. age of onset 3-6 years old diagnostic tests: 1. neurological exam 2. genetic testing(>120 GAA trinucleotide repeat)- gold standard 3. electromyography(nerve stimulation test) 4. echocardiography(due to hypertrophic cardiomyopathy being involved in Friedreich's ataxia) 5. EEG Treatment: no cure 1. anti-ataxic medication to manage symptoms(5-hydroxytryptophan, buspirone and amantadine) 2. physiotherapy(to help maintaining muscle function) 3. speech therapy case comments N3: in Freidreich's ataxia can be seen also: diabetic neurophaty and hypertrophic cardiomyopathy case comments N4: freidreich's ataxia: patho: disorder, where the mitochondria is impaired resulting in damage to various organ systems. the nervous system is damaged causing ataxia(abnormal, uncoordinated movement). this disorder also affects the pancreas and heart. normally, on chromosome 9, there's gene FXN, which encodes mitochondrial protein-Frataxin. the normal amount of Frataxin varies by tissue, with some tissues like the nervous system, pancreas and heart, containing lots of it. in Friedreich's ataxia, frataxin is decreased due to the mutation in FXN gene, which results in cell death. Friedreich's ataxia is caused by mutation in FXN gene, where there's an abnormal repetition of a GAA sequence within that gene. it is autosomal-recessive condition. its passed on by parents who are carriers. inheriting both copies of the FXN gene from each parent with an expanded GAA repeat is the most common way to get Friedreich's ataxia. onset: 10-3o years *FXN gene helps put together cofactorsL iron sulfur clusters

scenario N1: 21-year-old male, gate problem, bad memory, cranial nerve assessment normal. Plantar reflex abnormal, no fever, headache and drowsiness present, supple neck scenario N2: 21-year-old college boy, comes and complains of headache and dizziness. he is very active student and denies previous medical history. fever of 38, BP is normal and neck is supple(can be easily bent). his reflexes were normal except for plantar reflex(+4) 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

case commments N1: supple neck means no meningitis, it is seen in case of herpes symplex encephalitis localisation: brain parenchyma-panencephalitis-due to the infection and infla of the grey and white matter of the brain, inferior part of the frontal lobe and temporal lobe diagnosis: viral encephalitis caused by HSV(sporadic encephalitis) (for both scenarios) differential diagnosis: 1. viral encephalitis caused by HSV 2. tick borne enceohalitis 3. lethargic encephalitis 4. viral meningitis(herpes) case comments N2: viral encephalitis: classic triad: fever, headache, altered mental status raised ICP and focal neurological symptoms *because there is a mention of herpes symplex virus, maybe it is a "secondary encephalitis" due to post-infection from (HSV) alternatively, it could be allergic encephalitis bcz there is no mention of fever in the case diagnostic tests: 1. neurological exma 2. lumbar puncture 3. CT or MRI of brain treatment: AFN the main goals of treating enceohalitis are to treat symptoms and the cause of infla: 1. Anti-viral(acyclovir and famciclovir, 3000 mg), "patient will get better" 2. fluids may be given by IV if vomiting is severe 3. NSAIDs(corticosteroids)

epileptic seizures for 3 years, aura feeling. scenario 1: consciousness is impaired scenario 2: loss of consciousness or big epileptic seizure symptoms(tonic-clonic, myoclonic) 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: 1. medial part of temporal lobe 2. hippocampus 3. lateral surface of the lobe case comments N1: *if conciousness level is impaired it is not simple partial seizures(because conciousness is not lossed and it not impaired) *it is not generalized secondary partial seizures(conciousness is lossed, thats why it is complex partial seizures beacuse conciousness is impaired) *if conciousness is impaired it is the temporal lobe *if conciousness is not impaired it is frontal lobe- plus there is no sensory or motor manifestation Diagnosis: if scenario 1: consciousness is impaired- temporal lobe epilepsy(psychomotor epilepsy) scenario 2: loss of consciousness or big epileptic seizure -symptoms(tonic-clonic, myoclonic)-epilepsy *triggered by aura, visual hallucinations, taste disturbance *memory disturbance: DeJa'Vu Differential diagnosis: 1. temporal lobe epilepsy or epilepsy 2. brain tumor 3. TIA Diagnostic tests: 1. Electroencephalography(EEG)-test that detects abnormalities in brain waves and electrical activity in brain 2. MRI of brain(to detect tumor, to detect another causative pathology) treatment: first-line: anti-epileptic drugs(benzodiazepines-e.g. carbamazepine, valproic acid, lamotrigen-alternatives are phenytoin, gabaopentin, clonazapam 2. valproic acid and lamotrigen-alt. phenytoin, clonazapam, carbamazapine(contraindicated: ethosuximide) 3. valproic acid-alt. clonazapam, lamotrigen(contraindicated: phenytoin/ carbamazepine, gabapentin) 2. prevention: anticonvulsants(phenytoin) dependent on the type of seizures 3. epilepsy surgery: remove the causative factor of seizures, e.g. tumor case comments N2: epilepsy: a chronic disease of the brain, caused by recurrent spontaneous unprovoked paroxysmal attacks with motor sensory or psychic phenomena which are results hypersynchronic discharged of neurons/ pathophysiology: 1. Epileptiform neurons(<20%) 2. epileptic neurons(50%) 3. epileptic focus of brain(>90%) 4. epileptic focus on contralateral side(mirror focuses) 5. full epilepsy as a disease 6. epileptic brain classification: 1. partial seizures(local onset) a. simple partial seizures(without impairment or loss of consciousness) *characterized by: 1)motor jackson due to irritation of definite part of precentral gyrus in frontal lobe which cause in opposite side clinic seizures without loss or impairment of level of consciousness(LOC) 2) sensory jackson due to irritation of the definite part of postcentral gyrus in parietal lobe which causes in opposite side parasthesia b. complex partial seizures/temporal lobe epilepsy(with impaired consciousness) due to *irritation of structures of temporal lobe and limbic system characterized by psychomotor seizures(actions done without being aware of it), dejavu(seen already), dejaloo(read already) phenomena and impaired conciousness *what is common between simple partial and complex partial seizures: one focus(one part of brain is affected) and LOC c. generalised secondary partial seizures(focuses in both hemispheres) characterized by LOC with big epileptic seizures 2. generalised seizures(bil.symetrical without local onset)-myoclonic/clonic/tonic. toni-clonic 3. unclassified epileptic seizures(unknown reason) diagnosis: anamnesis of PT electroencephalogram EEC/MRI rule our lesions

an 83-year old woman with a history of hypertension and dyslipidemia developed acute onset of impaired speech and comprehension and right sided weakness. her previous medical history was notable for hyperthyroidism and a curative remote mastectomy for breast cancer. the patient was on 2 antihypertensive medications and a statin, and she wasn't receiving any antiplatelet medication. she was taken by ambulance to a primary stroke center. Initial exam showed global aphasia, right homonymous hemianopia, right hemiplegia and hemisensory loss. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: 1. left precentral and postcentrac gyrus 2. internal capsule(posterior limb) 3. Wernicke's area(temporal lobe) 4. Broca's area(frontal lobe 5. ICA diagnosis: acute ischemic stroke caused by distal left ICA occlusion, with salvageable penumbral tissue and persistant large vessel occlusion case comments N1: -right hemiplegia: damage can be in left central gyrus or motor cortex in frontal lobe or posterior limb of internal capsule -hemianesthesia: left postcentral gyrus on somatosensory cortex in parietal lobe or posterior limb of internal capsule case comments N2: global aphasia bcz: damage to both Brocca's and wernicke's which are responsible for both sensory and motor speech *bitemporal hemianopsia is: chiasm damage homonymous hemianopia: optic tract damage differential diagnosis: 1. ICA ischemic stroke 2. ICA hemorrhagic stroke 3. intracerebral hemorrhage 4. supratentorial lobe tumor diagnostic tests: physical exam lab tests CT with angiography multimodal brain MRI scan catheter cerebral angiogram echocardiogram continuous cardiac monitoring treatment: TEEL 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin

patient with mild scoliosis, pes cavus and hammer toes, mild dysarthria, gait disorder, falling 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: 1. posterior column(bulbothalamic tract) 2. lateral column(anterior/posterior spinocerebellar tract and lateral corticospinal tract) *caused due to genetic mutation of FXN gene, leading to GAA trinucleotide repeat of more than 120 times on chromosome 9, affecting frataxin case comments N1: CAG>/= 36x= Huntington dignosis: Friedrich's ataxia *maily affects younger population 10-30 years *damage to bulbothalamic= loss of deep sensation *damage to spinocerebellar tract= gait ataxia(loss of unconscious proprioception) *slurred speech and dysarthria(5 years after onces) *nonneurological: pes cavus/scoliosis/HOCM/diabetes differential diagnosis: 1. Friedreich's ataxia 2. Pierre-marie ataxia 3. charcot marie tooth disease(pes cavus and hammer toes present) 4. duschen muscular dystrophy diagnostic tests: 1. neurological exam 2. genetic testing(>120 GAA trinucleotide repeat)= gold standard 3. electromyography(nerve stimulatiomn test) 4. echocardiography(due to hypertrophic cardiomyophaty being involved in Friedreich's ataxia) 5. EEG treatment: no cure 1. anti-ataxic medication to manage symptoms(5-hydroxytryptophan, buspirone and amantadine) 2. physiotherapy(to help maintain muscle function) 3. speech theraphy

scenario 1: motor vehicle accident(MVA), can't remember anything, had contusion, severe headache, no peripheral reflex scenario 2: motor vehicle accident, can't remember anything, had confusion/compression, severe headache, normal plantar reflex 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: Scenario 1: brain parenchyma and anterior horns of the spinal cord(bcz: if patient has no peripheral reflex, areflexia, no plantar reflex- peripheral palsy, affected anterior horns) scenario 2: brain parenchyma(we do not write injury to anterior horn or spinal cord, if there is presence of plantar reflex) case comment N1: during car accident think about 3 things: 1. concussion an injury to the brain that results in temporary loss of normal brain function, clinical syndrome characterized by immediate and transient alteration in brain function, including alteration of mental status or level of consciousness, that results from mechanical force or trauma. 2. contusion bruising of brain tissue. When examined under a microscope, cerebral contusions are comparable to bruises in other parts of the body. They consist of areas of injured or swollen brain mixed with blood that has leaked from arteries, veins, or capillaries. Most commonly, contusions are at the base of the front parts of the brain, but may occur anywhere. 3. compression condition in which something increases the amount of pressure pushing on the brain, which can damage brain tissue. diagnosis: contusion of the brain and trauma/compression of spinal cord *contusion because severe amnesia. MVA there should be morphological deformity or injury *in MVA if location is unknown always write brain parenchyma *brain parenchyma contusion- memory loss and headache(increased ICP) *spinal cord injury(compression of anterior horns=peripheral palsy) Differential diagnosis: 1. contusion of brain and trauma(compression can be ruled out because there is no presence of lucid period(the period of time between regaining consciousness after a short period of unconsciousness) 2. epidural hematoma 3. concussion(brain or spinal cord) case comments N2:key words: morphological deformities due to MVA, severe amnesia, sever headache, assuming that the confusion is for a long period of time = they indicative of contusion Diagnostic tests: 1. X-ray craniography(he wants to hear this :D) 2. CT and MRI Treatment: 1. surgical resection of haematoma(contusion( in brain 2. surgery to relieve trauma/compression in spinal cord 3. conservative management(bed rest, fluids, pain relief, rehab) *brain parenchyma: brain tissue where function units are found which are neurons, cell bodies and glial cells

scenario 1: 21 year old man, has a gait, bad memory with 6th cranial nerve damage common symptoms include: confusion(about time, place and person), memory loss, poor balance and gait(ataxia) other info: alcohol, visual disturbances scenario 2: if plus those symptoms we find, confabulation, anterograde amnesia and retrograde amnesia 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: ? damage to: 1. mamillary bodies(if it will be scenario N2 only) 2. limbic system 3. hypothalamus 4. thalamus 5. cerebellum 6. brainstem case comments N1: peripheral ataxia seen in wernicke's korsakoff syndrome(WKS): you have damage of peripheral nerves and deep sensation fibers but not posterior or bulbothalamic tract diagnosis: scenario N1: Wernicke's encephalopathy(WE)(medical emergency as we need to prevent patient from WKS) 2. WKS *classic triad symptoms of Wernicke's encephalopathy(confusion, ataxia, nystagmus) *CN6 damage will present as lateral rectus palsy(nystagmus) differential diagnosis: 1. WE 2. WKS(only if there is confabulation, anterograde amnesia and retrograde amnesia) 3. vascular dementia 4. alzheimer's diagnostic tests: 1. blood and liver function tests(to check thiamine levels normal: 2.5-7.5 μg/dc) 2. CT or MRI(to check for degeneration of mamillary bodies) case comments N2: WKS is irreversible condition, rarely recovers, often requires support treatment Scenario 1: WE: 1. IV thiamine infusion(250-300 mg thiamine 2 timex a day for 3-5 days) 2. Give glucose but must make sure that the thiamine levels are normal scenario 2: WKS: Vitamin B1 tablets or injection. IV fluids (rehydration). Alcohol use disorder treatment. Nutritional support. Medications.

69-year-old woman has hypertension and diabetes melitus, she has weakness in her right arm and face(right side paresis) and this afternoon her husband said that she had drunken speech, drooping in the corner of her mouth and no loss of vision 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: MIddle and lower part of the precentral gyrus of the frontal lobe on left side and Broca's area diagnosis: cerebral ischemic stroke(due to occlusion of left middle cerebral artery due to emboli/thrombus) Case comments N1: *middle and lower part of the precentral gyrus- weakness in arm(middle) and face(lower) *damage to Broca's area(in frontal lobe)- drunken speech *no loss of vision- no internal capsule involvement Differentia diagnosis: 1. MCA ischemic stroke 2. MCA hemorrhagic stroke 3. Intracerebral Hemorrhage 4. subarachnoid hemorrhage 5. frontal lobe tumor case comments N2: *frontal lobe tumors(meningioma, gliomas and oligodendrocytomas) Lab diagnostic test: MRI with angiogram Treatment: 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin case comments N2: *is aspirin doesn't work use warfarin *1)Thrombolysis time frame is: within 0-4.5 hours onset of symptom 2)thrombectomy: more 4.5 hours but less than 6 hours more than 6 hours-anticoagulation and other risk factors or symptoms controlled *the Broca's area of frontal lobe is blood supplied by "middle cerebral artery". therefore, whenever patient has difficulty speaking, "MCA stroke" is most likely to be the correct diagnosis

Scenario N1: diplopia, morning stiffness and worsens at the time passes extra-ocular muscle not working, ptosis. no occulomotor damage. Scenario N2: patient has diplopia, drooping eyelid, muscle weakness with repetitive movement. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: acetylcholine(Ach) nicotinic receptors on post-synaptic membranes at the neuromuscular junction diagnosis: Myasthenia Gravis *MG is associated with abnormalities of the thymus, autoimmune hyperthyroidism *symptoms: ptosis, diplopia, muscle weakness case comments N1: complication: myasthenia crisis: accumulation of the Ach that is no able to bind bcz toxicity which may lead to coma of the patient. acute worsening of the symptoms can be caused by some other infection, respiratory failure, needs emergently respiratory support. differential diagnosis: 1. myasthenia gravis 2. lambert-eaton myasthenic syndrome 3. botulism 4. duschen muscular dystrophy diagnostic tests: 1. neurological exam 2. edrophonium chloride test(as known as Tensilon test) 3. blood test(to see the presence of abnormal antibodies) 4. electromyography treatment: *medications: 1. acetylcholinesterase inhibitors: pyridostigmine, blocks the nromal breakdown, increses lifetime and increases concentration of Ach 2.immunosuppressants: corticosteroids(prednisone) reduce the production of Antibodies *non-surgical treatment: 1. plasmapheresis: machine that filter out the attacking antibodies 2. Ig therapy: healthy antibodies is injected from donor *surgical treatment 1. thymectomy(it is believed the helper T cells that are produced in the thymus assist B cells in producing antibodies that attack the acetylcholine receptors in the postsynaptic cell). this surgery will only result in decreasing the sympt

scenario N1: a 7-year-old girl with a migraine is brought to your office by her mother, who is a patient of yours. she reports that her daughter has developed symptoms over the past 3 months. The headaches(HAs) are worse in the morning and have not responded to ibuprofen. in the past week, the HAs have been lasting longer(in fact, the girl has a constant HA now, worse still in the morning) and are now associated with vomiting. she has been missing school and complaining of blurry vision. her parents are separated and undergoing a divorce. her office exam prior to the visit was all for minor childhood ailments and she had met all the normal developmental milestones appropriately. exam : reveals normal vital signs. the child is rather quiet, but responds appropriately to commands. mild papilledema is noted as are bilateral CN 6 nerve palsies. motor and sensory exam are normal(Romberg cannot performed, see below) she is mildly dystaxic(but not dysmetric) on the left on finger-to-nose and heel-to-shin, and can not tandem walk. her gait is unsteady, and she stumbles as she walks. on standing still, she sways violently. deep tendon reflexes(DTRs) are symmetrically brisk. plantar testing is equivocal bilaterally. scenario N2: 7 year old with migraine for 3 months, papilledema(swelling of optic nerve), not responding to ibuprofen(NSAID), bilateral CN6 palsy. dysmetria in finger to nose test and heel to shin(dysdiadochinesia) 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: below the tentorium cerebelli affecting the: 1. cerebellum 2. roof of the 4th ventricle 3. pons(CN6) 4. medulla diagnosis: sub-tentorial tumor differential diagnosis: 1. sub-tentorial tumor 2. cerebellar hematoma(compresses the brainstem) 3. Hemorrhage in the posterior fossa 4. pineal tumor 5. hydrocephalus *case comments N1: don't write the actual tumor name, bcz it's a histological finding. for example medulloblastoma, astrocytoma, ependymoma, and so on diagnostic tests: 1. CT or MRI(preferred MRI) 2. brain biopsy(invasive) treatment: 1. surgical resection of the tumor, if it is a resectable area, followed by the cancer therapies 2. if not in a resectable area, continue with just the therapies(chemotherapy, radiation therapy, immunotherapy, and targeted drug therapy) case comments N2: how to access brain tumor: craniotomy where do you find the nuclei of CN- they are found in the roof. fibers of CN are always on the base CN7: fibers of it loops around the nuclei of CN6 in the pontomedullary junction before exiting case comments N3: general knowledge: there are 2 types of speech: 1. expressive/motor-integrated center for it is Brocca's area 44,45 frontal lobe 2. sensory/perceptive- the integrated center is Wernicke's area 22 temporal lobe case comments N4: *common cerebral symptoms: headache, dizziness, edema of the optic disc and etc. *local focal symptoms- due to the localization of the tumor *symptoms on distance far from pathologic process case comments N5: *tentorium cerebelli is a fold in the dura matter that splits the brain into a supra- and infratentorial part. above and below the tentorium respectively. *medulloblastoma arises infratentorially in the posterior fossa, usually affecting the cerebellum and the roof of the 4th ventricle. CSF flows from the lateral and 3rd ventricle into the 4th ventricle through the cerebral aquiduct. from there the CSF paths the subarachnoid space in the brain through the median and lateral apertures. it also drains into the central canal of the spinal cord

pilot jumps from plane, unconscious and after regaining consciousness he feels lethargic. positive meningeal symptoms, neck stiffness, fever, headache scenario 1:pilot/aircraft man+measles vaccine scenario 2: pilot/aircraft man+meningeal symptoms+ NO measles vaccine 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: brain parenchyma(affecting grey matter of cerebrum)-polioencephalitis diagnosis: meningoencephalitis *fatigue and lethargy(key symptom) accompanied by fever, headache irritability *neurological symptoms that can potentially develop ataxia, hemiplegia, seizures, infla of optic nerve(optic neuritis) differential diagnosis: 1. meningoencephalitis 2. tick borne encephalitis 3. lethargic encephalitis 4. viral meningitis case comments N1: if meningoencephalitis localization is leptomeninges+grey matter of cerebrum- brain parenchyma if lethargic encephalitis-only grey matter of cerebrum lab diagnostic tests: 1. neurological exam 2. lumbar puncture 3. CT or MRI treatment: the main goals of treating meningoencephalitis are to treat the symptoms and the cause of infla: 1. antiviral(acyclovir and famciclovir) 2. fluids may be given by IV if vomitibg is sevre 3. NSAIDs(corticosteroids) *depending of causative organism: you should give either *antibiotics if caused by bacterial or antiviral if caused by virus case comments N2: meningoencephalitis is very serious neurological condition resmbling both meningitis and encephalitis- infla of meninges(covering the CNS) and infla of the brain tissues respectively meningoencephalitis can be caused by bacteria, viruses, fungi and protozoan or as secondary sequel of other infla like AIDS. the viral or aseptic meningoencephalitis is mainly caused by enteroviruses, varicella-zoster viruses, herpes simplex viruses case comments N3: "encephalitis": infla of the brain tissue depending on the structure of the brain tissue that is affected, encephalitis can be divided into: 1. leukoencephalitis: ingfla of white matter of the brain 2. polioencephalitis: infla of grey matter of the brain 3. panencephalitis: infla of both white and grey matter of the brain

Scenario 1: a man met with a car accident, personality and mood changes more often, laceration on frontal lobe of face, contusion after 5 months, confusion, headache, lethargy, nausea, vomiting, rib fracture and damaged spinal cord, abdominal reflex absent, lower reflexes absent, neurological exam was normal scenario 2: Car accident laceration on face, frontal lobe, confusion after 5 months, contusion, headache, lethargy, nausea, vomitting, neurological exam normal. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: cerebral and subcortical areas diagnosis: post-concussion syndrome case comments N1: abdominal reflex: integrated centres: T6-T12. they are divided into 3 levels": 1.superior/upper superficial abdominal reflex- integrated centre is T6-T8; 2. middle superficial abdominal reflex- T8-T10; 3. lower superficial abdominal- T10-T12 absence of this reflex: pathology above 6 Differential diagnosis: 1. post-concussion syndrome 2. brain contusion 3. subarachnoid hemorrhage 4. brain tumor(supratentorial tumor) case comments N2: key words indicating post-concussion syndrome are: *mood changes(depression) *chronic headaches *confusion, decrease/absence of reflexes plus presence of pathological reflexes. *and the fact that patient had car accident 5 months ago and symptoms developed after that Diagnostic tests: 1. History of head injury 2. presence of post-concussion syndrome(PCS) symptoms 3. X-ray, CT/MRI of brain and spinal cord, craniography Treatment: 1. targeted therapies to treat PCS symptoms 2. supportive care: bed rest, medications(analgesics), fluids case comments N3: *abdominal reflex: can be tested by ligtly stroking the abdominal wall diagonally towards the umbilicus in each of the 4 quadrants of the abdomen. *reflex contracttions of the abdominal wall are absent in upper motor neurone lesions above the segmental level

62 year old female, conscious but mildly confused with history of TIA. Arterial pressure is high. Face is drooping on one side of face. Half side facial palsy. Abducens palsy(nose rest position) and contralateral hemiplegia. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: damage to the base of the brainstem at the level of pons, affecting CN6 and CN7(presenting as "Fonville's alternative syndrome) case comment N1: *damage to base of pons- facial and abducens nuclei palsy *babinski absent= negative babinski= normal= plantar response diagnosis: lacunar infarct of the pontine arteries, lacunar ischemic stroke case comments N2: *the symptoms presented in the case history is classic for "foville's alternative syndrome", but DO NOT ever write that under diagnosis(cz this is symptom, not diagnosis) *peripheral facial and abducens palsy with contralateral central hemiplegia- "foville's alternative syndrome" *occlusion of pontine arteries which arise from basilar artery case comments N3: key wordS: facial palsy(CN7), abducens palsy(CN6), contralateral hemiplegia differential diagnosis: 1. lacunar infarct of the pontine arteries, lacunar ischemic stroke 2. subtentorial tumor 3. brainstem hemorrhage 4. vascular malformation(arteriovenoius malformation) lab diagnostic tests: 1. neurological exam of CN6 and CN7 2. CT and MRI with angiography treatment: 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin

a 80 year lod man presents with acute visual loss. he reports difficulty seeing objects on his right side. his wife said he also reports seeing people whoa are not in the room. on exam, there are no motor or sensory deficits. visual fields are shown below(black=no vision) 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: infarct of left occipital lobe and left visual cortex due to occlusion of posterior cerebral artery(PCA) affecting the calcarine artery branch(left sulcus calcarinus of the occipital lobe and left visual cortex) diagnosis: PCA ischemic stroke(affecting calcarine artery) on the left side case comments N1: *occipital lobe(primary vision centre) *calcarine branch-supplies the visual cortex case comments N2: key word is ACUTE visual loss: it wule outs tumors and is more indicative of stroke: -patient right side affected- meaning the left lobe will be affected -visual cortex is in the occipital lobe -the occipital lobe is mainly supplied by PCA -stroke can sometimes lead to hallucination and delusions- "seeing people who are not in the room" differential diagnosis: 1. PCA ischemic stroke(affecting calcarine artery) 2. Intracerebral hemorrhage 3. PCA hemorrhagic stroke 4. occipital lobe tumor lab diagnostic tests: 1. CT scan with angiogram 2. coagulation parameters treatment: TEEL 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin case comments N2: PCA stroke: -posterior portion of brain -visual cortex -visual hallucinations -visual agnosia(seeing things but can't recognize) -contralateral hemianopia with macular sparing case comments N3: homonymous hemianopia *left PCA stroke: -left optic tract lesion -right visual loss *right PCA stroke: -right optic tract lesion -left visual loss *contralateral homonymous hemianopsia- lesion at the optic tract case comments N4: *visual cortex is found in the occipital lobe calcarine sulcuse and broadmann area 17 *what is the difference between optic nerve and optic tract: optic nerves contains fibers from one eye- but the tract contains fibers from both the eyes. *in this section If you think its tumor: is there any weight loss this case mentions acute visual loss hence its more likely to be stroke-gradual onset would be most likely a tumor case comments N5: why it is homonymous hemianopia not cortical blindness: because the left PCA has been affected

a 75-year old man presents with acute loss of ability to move his right hip and leg. on exam, he has decreased sensation to pinprick and vibration of his right leg. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: left precentral gyrus(upper part) and left postcentral gyrus(apper part)- due to occlusion of the left Anterio Comunicatin artery(ACA) diagnosis: ACA ischemic stroke on the left side * left precentral gyrus(frontal lobe)- loss of ability to move his righte leg *left postcentral gyrus(parietal lobe)- sensory loss in the right leg(superficial and deep) differential diagnosis: 1. ACA hemorrhagic stroke 2. Intracerebral hemorrhage 3. subarachnoid hemorrhage 4. frontal lobe tumor case comments N1: why is the diagnosis ACA? -we can exclude MCA bcz the "Broca's area is not affected, there is no speech problems -we can exlude anterior cerebral artery, bcz it supplies just the frontal lobe, meaning problem will be just motor -ACA bcz: it supplies the superior frontal and anterior parietal, meaning it cause damage to both motor and sensory systems without affecting speech Lab diagnostic tests: CT with angiography treatment: TEEL 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin case comments N2: *decrease sensation to pin prick= pain= superficial sensation= later spinothalamic tract *decreased sensation to vibration= deep sensation=bulbothalamic tracts(posterior column) *loss of ability to move= primary motor cortex(frontal lobe) precentral gyrus in upper part

a 50 year old woman presents vertigo, dizziness, numbness of the right side of the face, confused, but answers questions without mistakes. attempted vomiting. history of disease includes: several ischemic attacks in last 2 weeks exam: state of consciousness, orientation in date and time and place arenormal. voluntary movements of limbs are good, but on the left side observed: dysmetria+ intention tremor on the left side observed nystagmus, ptosis and miosis superficial sensation modalities are lost on the right side of the face in the trunk and limbs on the opposite side. reflexes on both sides are normal as strength in the right limbs(in the left extremities muscle tone is decreased). no plantar response present 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: left superior cerebellum and midbrain diagnosis: superior cerebellar artery(SCA) ischemic stroke on the left side case comments N1: *in this case we don't have dysphagia and dysarthria, and for this reason we excluded PICA *key sentence: superficial sensation modalities are lost on the right side of the face, in the trunk and limbs on the opposite side differential diagnosis: 1. SCA ischemic stroke 2. SCA hemorrhagic stroke 3. Intracerebral hemorrhage in posterior fossa 4. cerebral tumor of posterior fossa diagnostic tests:CT with angiogram treatment: TEEL 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) BP Should be less than 185/110 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin case comments N2: the cranial nerve nuclear are horizontal structures spread out in the midbrain(3,4), the pons(5,6,7,8) and the medulla(9,10,11, 12)

polioenchephalitis, prostate hyperplasia, neck stiffness, all senses intact, fever, meningismus, sinusitis, BP 210 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: leptomeninges(pia, arachnoid matter and CSF) in the brain and spinal cord, due to infla diagnosis: secondary purulent streptococcal pneumonial meningitis(caused by streptococcus pneumonia bacteria)- ask for CSF paper before giving clinical diagnosis case comments N1: *meningeal symptoms *sinusitis is caused by streptococcus pneumonia bacteria and transmission through oral or nasal causing respiratory infections differential diagnosis(ask for CSF paper before giving clinical diagnosis): 1. secondary purulent streptococcal pneumonial 2. secondary serous tuberculosis meningitis 3. viral serous meningitis(varicella zoster, herpes simplex virus) 4. encephalitis(viral, tick borne) diagnostic tests: 1. lumbar puncture between L3-L4(spinal tap) 1) turbidity 2) increased CSF pressure(>180 mmH20 in supine position and >200-300 mmH20 in sitting position) via Bullit's manometer. if there is no manometer, count the drps that come out from the needle. >60.70 drops/min= increased CSF pressure 3) pleocytosis(usually of polumorphonuclear(PMN) leukocytes); WBC counts> 10 cells/mm3 4) decreased glucose concentration(<45 mg/dl) 5) increased protein concentration(>45 mg/dl) 2. check meningeal signs: Kernig, Brudzinski and nuchal rigidity treatment: 1. antibacterial therapy in 1st hours of the disease(cephalosporins 3rd generation, oral ceftriaxone 4 mg/day or IV meronem 3 mg/day) 2. osmotic diuretics to decrease ICP(mannitol)- give osmotic to all purulent meningitis 3. dexamethasone to reduce infla 4. normalisation of vital signs

scenario N1: 50 year old woman, irregular movements of hands and legs, increased tone of limbs, dystonia(torsion dystonia) used to forget daily work, slow thinking, speech issues scenario N2: 46 year old man, deteriorative cognitive function, started to think slowly , speech problems, personality changes, fidgeting at night, memory loss 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: neurodegeneration of caudate nucleus and putamen in the basal ganglia *caused due to genetic mutation of Huntingtin gene, leading to CAG trinucleotide repeat of more than 36 times on chromosome 4 case comments N1: CAG- cystosine, adenosine, Guanine- huntigton protein diagnosis: Huntigton disease differential diagnosis: 1. huntington disease 2. parkinson disease 3. alzheimer disease 4. willsonism diagnostic tests: 1. genetic testing(>36 CAG trinucleotide repeat)- gold standard 2. MRI to see atrophy of the caudate nucleus treatment: there is no cure for this disease as it is a progressive neurodegenerative disease. best thing to do is treat the symptoms. 1. physical therapy 2. dopamine inhibitors case comments N2: caudate nucleus and putamen(caudate+putamen=striatum)

52-year-old woman, history of TIA, one sided face drooping, hypertension. Neural exam shows CNVII and CNXII palsy. right sided hemiparesis and hemiplegia. 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: posterior limb and knee of internal capsule on left side cerebral ischemic stroke(due to occlusion of lenticulostriate artery which is branch of the MCA due to thrombosis or emboli)(internal capsule ischemic stroke(MCA-LSB) Diagnosis: Lenticulostriate artery(branch of MCA) ischemic stroke on the left side *lenticulostriate artery supplies the posterior limb and knee of the internal capsule *through the posterior limb of internal capsule travels the: spinothalamic, bulbothalamic and corticospinal tract *through the knee of internal capsule travels the: corticonuclear tract *damage to corticospinal tract -hemiplegia/ hemiparesis *damage to the corticonuclear tract- CNVII and CNXII central palsy because the corticonuclear tract damaged Differential diagnosis: 1. Ischemic stroke of MCA 2. Haemorrhagic stroke of MCA 3. Frontal lobe tumor Diagnostic tests: CT with angiography Treatment: 1. thrombolytic(IV TPA-tissue plasminogen activator within 3 hours 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. Long term management-aspirin

Scenario 1: 26 year old woman, admitted to hospital, consfused with CNVII and CNXII palsy and contralatera hemianesthesia and hemiplegia. She has a history of TIA. Scenario 2: right tongue deviation, right sided facial drooping, hemiplegia, hemianesthesia, history of TIA, high arterial pressure 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: posterior limb and knee of internal capsule on left side cerebral ischemic stroke(due to occlusion of lenticulostriate artery which is branch of the MCA due to thrombosis or emboli)(internal capsule ischemic stroke(MCA-LSB) Diagnosis: Lenticulostriate artery(branch of MCA) ischemic stroke on the left side case comments N1: *to differentiate between hemorrhagic vs ischemic stroke: in hemorrhagic you will have increased ICP, and associated symptoms include Cushing reflex(resulting in the Cushing triad of widened pulse pressure (increasing systolic, decreasing diastolic) bradycardia, and irregular respirations), vision loss, etc. case comments N2: *lenticulostriate artery supplies the posterior limb and knee of the internal capsule *through the posterior limb of internal capsule travels the: spinothalamic, bulbothalamic and corticospinal tract *through the knee of internal capsule travels the: corticonuclear tract *damage to corticospinal tract -hemiplegia/ hemiparesis *damage to spinothalamic and bulbothalamic tract-hemianesthesia(cerebral, conductive global hemianesthesia) *damage to the corticonuclear tract- CNVII and CNXII central palsy because the corticonuclear tract damaged Differential diagnosis: 1. Lenticulostriate artery(branch of MCA) ischemic stroke 2. 1. Lenticulostriate artery(branch of MCA) hemorrhagic stroke 3. Ischemic stroke of MCA 4. Haemorrhagic stroke of MCA 3. Frontal lobe tumor Diagnostic tests: CT with angiography Treatment: 1. thrombolytic(IV TPA-tissue plasminogen activator within 3 hours 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. Long term management-aspirin*damage to spinothalamic and bulbothalamic tract-hemianesthesia(cerebral, conductive global hemianesthesia) case comments N3: *why is internal capsule damaged: according to his symptoms: contralateral hemianesthesia and hemiplegia it is not cerebral cortex bcz in that case should be having: cerebral cortical dissociation. *It is internal capsule, posterior limb of the tracts involve which are: lateral corticospinal, bulbothalamic, lateral spinothalamic. *also knee of the internal capsule bcz the cortical bulbar or cortical nuclear tract is affected.

Scenario N1: 60 year old woman is brought by ambulance, dysarthria, swallowing problem, vertigo, dizziness, numbness- left side of face. previous history of ischemic attacks Scenario N2: 60 year old woman is brought by ambulance to ED with complaints of impaired speech and swallowing, vertigo, dizziness, numbess of the left side of the face. She is little confused, but answers all questions without mistakes. the nurse states, that she attempted vomitting. history of disease include several TIAs last 2 weeks. exam: state of consciousness, orientation in date and place are normal, nbut speech is impaired-dysarthria. Voluntary movements of limbs are good but on the left side observed dysmetria and intention tremor. Superficial sensation modalities are lost on left side of face and in the trunk and limbs on the opposite side. Gag reflex is decreased, soft palate is not contacted on the left side, on the same side also observed nystagmus, ptosis and constricted pupil. Reflexes on both sides are normal as strength in the right limbs(in the left extremities muscle tone is decreased). no plantar response is present 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: right posterior inferior cerebellum and medulla diagnosis: posterior inferior cerebellar artery(PICA) ischemic stroke on the right side case comments N1: *damage to spinal trigeminal nucleus- ipsilateral numbness of face(pain and T sensation) *damage to vestibular nuclei- dizziness and vertigo *damage to the nucleus ambigus- difficulty in swallowing and dysarthria(CN IX and XI) differential diagnosis: 1. posterior inferior cerebellar artery(PICA) ischemic stroke 2. posterior inferior cerebellar artery(PICA) hemorrhagic stroke 3. intracerebral hemorrhage in posterior fosaa 4. cerebral tumor of posterior fossa diagnostic tests: 1. neurological exam 2.CT with angiography treatment: 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin case comments N2: *dysarthria-CN7(pons), CN9 and CN12- medulla *dysphagia+gag reflex- CN9, CN10- medulla *numbness in face-CN5-pons *Dysmetria+intention tremor-cerebellum *nystagmus, ptosis, miosis-CN3-midbrain the problem here mainly affects the medulla/pons and the cerebellum, which is supplied by PICA *If it affects the pons, midbrain it is AICA case comments N3: horner's syndrome: 1. ipsilateral sensory loss(face)-ptosis, miosis 2. contralateral sensory loss(limbs) 3. ipsilateral laryngeal and pharyngeal paresis

a 45-year old mechanic presents with voice hoarseness, no gag reflex and difficulty swallowing. on observation, he has right eye miosis, right eyelid dropping, loss of pain and T in the right side of the face. Patient also had vertigo, nystagmus, dysarthria and right-hand ataxia. his left hand has loss of pain and T(including the trunk). 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: right posterior inferior cerebellum and medulla diagnosis: posterior inferior cerebellar artery(PICA) ischemic stroke on the right side case comments N1: *presenting as lateral medullary syndrome *infarct of nucleus ambiguous(CN9 AND 10)=dysphagia, voice hoarseness and no gag reflex and difficulty in swallowing\ *infarct descending sympathetic fibers=miosis and ptosis *infarct of spinal trigeminal nucleus= ipsilateral right side face loss of pain and T *infarct of vestibular nuclei= vertigo and nystagmus *infarct of inferior cerebellar peduncles= ipsilateral right hand ataxia *infarct of the lateral spinothalamic tract= left hand loss of pain and T differential diagnosis: 1. posterior inferior cerebellar artery(PICA) ischemic stroke 2. posterior inferior cerebellar artery(PICA) hemorrhagic stroke 3. intracerebral hemorrhage in posterior fosaa 4. cerebral tumor of posterior fossa diagnostic tests: 1. neurological examination 2. CT with angiography treatment: 1. Thrombolytics(IV TPA -tissue plasminogen activator within 3 hours) 2. embolectomy(removal of clot within 8 hours) 3. endovascular stenting 4. long term management- aspirin

7 year old with dysarthria, double vision, and problem with nerve conduction 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: white matter of brain and spinal cord due to the destruction of oligodendrocytes forming the glial scars *anterior cyrcle of lateral ventricles *paraventricular area *corpus callosum *cervical intyusdjy C5-T2 *lateral and posterior of the spinal cord *brainstem *cerebellum diagnosis: multiple sclerosis case comments N1: multiple sclerosis most commonly affect the white matter in the optic nerve, brainstem, cerebellum, corpus callosum(largest white matter structure in the brain) and spinal cord, or white matter tracts close to the lateral ventricles. but MS has also been shown to affect the less myelinated regions closer to the surface of the brain, known as cortical grey matter. Damage to both white matter and grey matter structures are linked to cognitive impairement differential diagnosis: 1. MS 2. tRANSVERSE MYELITIS 3. acute disseminated encephalomyelitis(ADEM) 4. Amyotrophic lateral sclerosis(ALS) diagnostic tests: 1. blood tests: to rule out other diseases like MS 2. Spinal tap: to observe abnormalities in CSF(e.g. antibodies), that may potentially indicate MS 3. MRI(gold standard): MRI can reveal lesions(presented as whitish shade) caused by MS, "oval shaped" and greater than 6 mm in size. Gadolinum contrast injected IV can highlight active lesions from older lesions, via the newly formed "GLIAL SCARS" treatment goals for treatment/management of MS *reduce number of repalses and prolong remission *shortening and decreasing frequency of exacerbations *relieving symptoms *delaying disability, especially patient's ability to walk treatment of MS attacks: 1. corticosteroids: anti-inflamatory and immunosuppressant 2. plasmapheresis: filters blood to remove harmful antibodies 3. interferon 4. for chronic progressive: ocrezumab, tedanifir

23-year-old aircraft man, concussion 3 years ago, no post-concussion syndrome. sudden fall and loss of consciousness for 5 minutes. the next day diffused headache, papilledema, meningismus, shaking body. admitted to hospital and patient was responding to verbal command, bilateral babinski, diplopia, 6th nerve palsy. measles vaccine. scenario 1:pilot/aircraft man+measles vaccine scenario 2: pilot/aircraft man+meningeal symptoms+ NO measles vaccine 1. Localization 2. Tests 3. Differential diagnosis 4. Diagnosis 5. Prognosis and Treatment

localization: white matter of brain parenchyma and spinal cord due to inflammation and demyelination comments: "pilot/aircraft man+measles vaccine= ADEM "pilot/aircraft man+meningeal symptoms+ NO measles vaccine= meningoencephalitis diagnosis: Acute Disseminated Encephalomyelitis(ADEM) *ADEM is caused postvaccinal(post infectious encephalitis) *papilledema, diplopia, inflammation of the brain parenchyma mainly white matter and 6th nerve palsy is seen in ADEM *diffuse headache(cerebral symptom due to increased ICP) Differential diagnosis: AMOO 1. acute disseminated encephalomyelitis(ADEM): acute=rapid, disseminated= many place, encephalomyolitis= foci in brain and brainstem and spinal cord 2. multiple scperosis 3. optic nerve glioma 4. optic neuritis Diagnostic test: 1. MRI(in ADEM, MRI will show diffuse, poorly demarcated,(>1 to 2 cm) lesions involving predominantly the cerebral white matter. in MS, MRI will reveal lesions(presented as a whitish shade), "oval shaped" and greater than 6 mm in size 2. lumbar puncture(aid in eliminating other cause) treatment: 1. IV methyl prednisone(corticosteroids(immunosuppressant) 2. IV IgG from healthy donor 3. plasmapheresis demyelinating disorders due to the antigen challenge (infection or inflammation) about ADEM: ADEM is neurological, immune mediated disorder in which widespread inflammation of the brain and spinal cord damages tissue known as white matter. white matter is tissue composed of nerve fibers, many of which are covered by a collection of fats and proteins known as myelin causes and risk factors: autoimmune disease(probably). could be reaction to an infection. mostly, the attacks happens when a child is getting over a common illness, like a cold or stomach bug. ADEM sometimes follows a vaccine, especially certain rabies shots and the vaccine for measles, mumps and rubella. but researches found no direct link. from pic: ADEM is monophasic inflammatory demyelinating disorder that characteristically begins within 6 weeks of an antigenic challenge such as infection or immunization. it occurs more often in young and causes rapid development of multifocal or focal neurological deficits, perivenous inflammation, edema and demyelination are the pathological hallmarks of ADEM. these lesions commonly enlarge and coalesce, forming lesions pathologically indistinguishable from MS. epidemiology and risk factors: ADEM can occur at any age but perhaps because of the higher frequency of immunization and exposure to new antigen, it is most common during childhood. unlike MS, both sexes are affected with equal frequency. no association has been noted with pregnancy. clinical features: a prodrome of headache, low-grade fever, myalgia, and malaise often precede the onset of ADEM by a few days. the most frequent clinical signs are motor deficit, followed by sensory deficits, brainstem signs, and cerebellar signs. CSF findings are variable, normal results were present upn to 70 % of patients. oligoclonal bands were positive in over 60 %. neurological symptoms develop rapidly in the acute phase and are commonly associated with encephalopathy, stupor, coma, meningismus, and seizures. peak severity occurs within several days and recovery may begin soon afterward. the prognosis for recovery is often quite good. treatment: with IV methylprednisolone leads to stop of the disease progression and allows sooner recovery, just as with MS. plasma exchange can be tried in those with severe deficits and little response to corticosteroids, IV IgG has been used successfully.