Neurology

Penumbra

Area with salvagable potentia via thrombolytics, larger penumbra=better outcome

Post-Concussion

Closed Head Injuries Complex disorder in which symptoms last for weeks or months after the injury that caused the concussion Symptoms occur within the first 7-10 days after injury and resolve within 3 months- Can persist for years Etiology: May occur due to structural damage to brain or disruption of neurotransmitters, Also, can be due to psychological factors RF: older age, women, trauma (car accidents, sports, assaults, falls) Presentation: Headaches, dizziness, fatigue, irritability, anxiety, insomnia, loss of concentration, memory loss, noise & light sensitivity, behavior/emotional changes (irritable, suspicious, argumentative, or stubborn) Dx: CT, MRI Tx: symptomatic

Myoclonic Seizures

Seizure Disorders: Generalized Seizures Brief jerking movement, localized or generalized, associated mainly with rare neurologic conditions, anoxia

Atonic Seizures

Seizure Disorders: Generalized Seizures Loss of posture ('drop attack')

Absence (Petit mal) Seizures

Seizure Disorders: Generalized Seizures RF: Always begin in childhood, end by age 20, spells can be induced by hyperventilation Presentation: Brief loss of consciousness, minimal motor symptoms (eye-twitching), "stare into space," look like daydreaming, unaware of attack, no post-ictal state Dx: EEG- 3-Hz generalized spike-wave discharges, must be differentiated from complex partial seizures

Clonic Seizures

Seizure Disorders: Generalized Seizures Rhythmic twitching of the body, associated with LOC

a

A 12-year-old boy presents after waking with a new onset of left hemiparesis. He is also experiencing slurring of speech, double vision, numbness of the face, dizziness, neck pain, and headache. His cognition is normal. He had been playing hockey on the evening prior to presentation and was struck by a puck on his neck. He has no significant past medical history. On physical examination, blood pressure is 110/60 mmHg, pulse 72/minute, and respirations 16/minute. His heart sounds and breath sounds are normal. The power in the left upper and lower limbs is 3/5, with sensory loss on the left side of the face and arms. What caused the boy's hemiparesis? a. Stroke due to carotid dissection b. Cervical cord injury c. Brachial plexus injury d. Transverse myelitis

c

A 19-year-old male presents with a chief complaint of sudden onset of vomiting, headache, vision changes, numbness and tingling of extremities, difficulty speaking, difficulty writing, loss of coordination, and loss of balance. His past medical history is significant for sickle cell anemia. Physical exam findings are consistent with acute cerebrovascular insufficiency. Early detection and prevention of stroke in sickle cell anemia is now possible by using screening tests. Which of the following imaging modalities is recommended as a screening test for cerebrovascular disease/stroke in sickle cell disease (SCD) patients? a. MRI b. CT c. Transcranial Doppler Ultrasonography d. Neurocognitive testing

b

A 34-year-old male presents with muscle weakness, lack of coordination, and tingling in his fingertips; he states that he has not been able to control his urinary function for the past few weeks. He also states that he has double vision sometimes. Which of the following conditions is the most likely diagnosis for this patient? a. Parkinson disease b. Multiple sclerosis c. Multiple myeloma d. Stroke

c

A 24-year-old woman, who has been consuming a strict total vegan diet (without dairy products or eggs) for the past 8 years, presents with a 2-week history of persistent fatigue and decreased functional capacity. She also gives history of numbness and pins and needle sensation in her feet for the past 3 weeks. The patient is having other problems, such as increased irritability and forgetfulness. Physical exam reveals pallor, peripheral neuropathy of her lower extremity, and memory deficits. CBC shows a macrocytic, normochromic anemia. There is also an elevation in the levels of methymalonic acid and homocysteine. Which of the following therapies is indicated for this patient? a. Folate supplementation b. Iron supplementation c. Vitamin B12 supplementation d. Erythropoietin therapy

c

A 27-year-old African-American male is seen in the emergency room for generalized seizures. You are informed that the patient was with his wife when he had a seizure in the kitchen of his home and then experienced two more seizures within the span of 30 minutes. The paramedics on arrival administered 10mg of diazepam intravenously. En route to the emergency room the patient suffered an additional seizure in the ambulance. Further information from the wife revealed a past medical history of latent tuberculosis infection (LTBI) for which the patient was being treated with isoniazid (INH). His physical exam demonstrates a post-ictal patient who is responsive to painful stimuli. His vitals are 150/110 mmHg, pulse 110/minute, respirations 24/minute, and temperature of 98.2 Fahrenheit (36.6 Celsius). His pupils are reactive to light and there is no nystagmus. His lung and cardiac examinations are normal. His abdomen is soft and nontender. There is no evidence of cyanosis or needle tracks and his neurological exam is grossly intact. His pulses are intact. Lab work includes: Hemoglobin 16mg/dL Hematocrit 48% White cell count 18x109/L Sodium 140mEq/L Potassium 4.9mEq/L Chloride 100mEq/L Bicarbonate 7mEq/L Blood Urea Nitrogen 20mEq/L Creatinine 2.0mEq/L His blood gas is 6.99 / pO2= 112 / pCO2= 45. His electrocardiogram demonstrates a sinus tachycardia without ectopy or ischemia. The chest X-ray is normal. The toxicology screen is pending. Sodium bicarbonate is given to correct the acidosis along with benzodiazepine and phenytoin. The seizure activity does not stop and the patient is eventually intubated. (Fill in the blank): The next therapeutic step would be to __________________________. a. Administer calcium gluconate IV b. Administer sodium thiosulphate IV c. Administer pyridoxine (Vitamin B6) IV d. Administer glucagon therapy IV

c

A 31-year-old male with a known generalized seizure disorder is brought to your rural emergency department at 11:00PM on a Saturday night. He is brought in by his friends who state that the patient "had a seizure and did not wake up." When he did not wake up after 30 minutes, his friends called '911'. On examination, he is breathing and his heart is beating. He is warm, dry, and pink. His basic laboratory values are within normal limits, and the non-contrast CT scan of his brain is unremarkable. An emergency electroencephalogram (EEG) is not available. His only medications are phenytoin and phenobarbital. After receiving the initial laboratory and diagnostic test results, which of the following interventions is the most appropriate next step in the treatment of this patient? a. Glucose b. Phenobarbital c. Lorazepam (Ativan) d. Phenytoin (Dilantin)

d

A 55-year-old male architect starts to develop behavioral and mental changes. In addition, he is having coarse, spasmodic, involuntary movements, which involve his face and his extremities. What is the classification of this abnormal movement? a. Cogwheel rigidity b. Athetosis c. Asterixis d. Chorea

a

A 33-year-old man complains of severe thirst and frequent urination gradually developing over 1 month. He claims to consume more than 8 liters of fluids per day but despite that fluid intake, he states that he "is always thirsty." Fasting blood glucose is 90 mg/dL. On brain MRI, the hyperintensity of the posterior pituitary is absent. Central diabetes insipidus is suspected. Which of the following drugs is used to treat this patient? a. Desmopressin b. Verapamil c. Propanaolol d. Triamterene e. Digoxin

d

A 34-year old man presents with a right-sided periorbital headache of 20 minutes duration. The pain is described as excruciating and bore-like, and is associated with tearing and redness of the right eye, right eyelid swelling, and nasal congestion. The headaches have been occurring at multiple times nearly daily over the past two weeks, each episode lasting approximately 30 to 60 minutes. The pain is not relieved with acetaminophen or ibuprofen. There is no nausea, vomiting, or photophobia. There is no history of amaurosis, visual scintillations, diplopia, focal weakness, numbness, neck stiffness, or other common neurologic complaints. The patient has had similar bouts of headaches over the past five years, the duration of which has been three to four weeks. The patient has an otherwise unremarkable medical history. General exam is remarkable for right eye conjunctival injection. The neurologic exam is significant for a mild right ptosis; the right pupil is 2 mm and reactive to light; the left pupil is 4 mm and reactive to light. There are no other neurologic findings. Which of the following is the most effective abortive therapy for this patient's headache? a. Aspirin b. Meperidine c. Naproxen d. Nasal oxygen

a

A 34-year-old male is admitted to the hospital following loss of consciousness. The patient had been ill with fever and headache for several days, then developed double vision, confusion, and loss of consciousness. He has been otherwise healthy with no past medical conditions. Imaging reveals edema of the frontal lobe. Which of the following viruses is the most common cause of this patient's condition? a. HSV b. West Nile virus c. Adenovirus d. EBV

NIH Stroke Scale (NIHSS)

A 42 point scale used to assess the severity of stroke

b

A 42-year-old female presents with a 7-day history of pain in her right arm. The patient denies any trauma or injury to this extremity just prior to the pain starting, but she does admit to having a Colles' fracture in this arm around 2 months ago. She denies any injury to her back, neck or other musculoskeletal system prior to the event of pain. She describes the pain as burning and throbbing with an extremely diffuse, uncomfortable aching accompanying it. She further states that this limb has become extremely sensitive to touch and cold; it does appear somewhat more swollen than her left arm. The patient is very upset; she does not know why her arm is so painful when she has not done anything to it. She is a nonsmoker. She does not drink alcohol, and exercises 3 times a week. Physical examination conducted of the extremity reveals a slightly cyanotic, mottled right arm with generalized pain of the entire extremity. Pulses are faint (1+) and ROM is limited. Radiograph studies are obtained and reveal spotty areas of apparent osteopenia of the right upper extremity. Which of the following conditions is the most likely diagnosis for this patient? a. DVT b. Complex regional pain syndrome c. MS d. Fracture

b

A 46-year-old HIV-positive male starts to develop headaches. At first, he attributes the headaches to stress. However, they persist and become worse over the next few weeks. He develops nausea and vomiting, and he thinks he has a fever. He starts to become confused, so he seeks medical attention. On physical examination, his temperature is 100°F. He has signs of meningeal irritation. A lumbar puncture is performed, and there is an elevation of his CSF pressure. Cerebrospinal fluid is sent to the lab. The CSF is centrifuged. A drop of India ink is placed on the slide along with a drop of the spun CSF. The India ink test is positive. Which of the following clinical findings may likely be present in this patient? a. Babinski's sign b. Kernig's sign c. Chvostek's sign d. Kussmaul's sign

d

A 65-year-old woman presents to the hospital complaining of morning stiffness and associated bilateral shoulder pain for the past month. She reports that she has also lost several pounds over the past month without intentionally dieting. The physical examination is essentially normal. Which of the following laboratory or diagnostic test results would you expect to find? a. Elevated CK b. Microcytic hypochromic anemia c. Abnormal EMG d. Elevated CRP

c

A 52-year-old male was found unconscious in a park. On physical examination, his vital signs are a pulse 90/minute, blood pressure 140/90, respiratory rate 24/minute. He appears disheveled and smells of alcohol. Noisy respirations with a weak gag reflex are noted. A bottle of wine is found in his pocket, he has an old scar on his forehead, and there is a 2-week-old sutured laceration in his scalp. His right pupil is 6 millimeters and dilated. His left pupil is 3 millimeters. He responds only to noxious stimuli, and he moves the left side of his body more than the right. Based on this information, which of the following interventions is the next step in the management of this patient? a. Administer naloxone 2 mg iV b. Head CT c. Secure an airway d. Administer thiamine 100 mg IV push

a

A 62-year-old man with hypertension presents with sudden onset of right eye blindness while shaving this morning. He describes a "curtain falling over my right eye," which cleared spontaneously after 10 minutes. He had no other concurrent neurologic symptoms and no prior episodes of similar description. His general examination reveals a blood pressure of 140/90 mmHg, but it is otherwise unremarkable. Neurologic exam is normal. Based on this information, what is the most likely diagnosis for this patient? a. Right internal carotid artery transient ischemic attack (TIA) b. Basilar artery TIA c. Left posterior cerebral TIA d. Left internal carotid artery TIA

b

A 65-year-old woman comes to your office complaining of general weakness, which gets worse as the day progresses, since the the symptoms first started several days ago. She says she has been having double vision and you notice her poor posture. A blood test reveals presence of antibodies to acetylcholine receptor. Repetitive nerve stimulation test showed a decremental response. What is the diagnosis in this patient? a. Chronic fatigue syndrome b. Myasthenia gravis c. SLE d. Duchenne's muscular dystrophy

a

A 72-year-old African-American male has a past medical history that is significant for severe and uncontrolled hypertension; he is brought into the emergency room by his family due to a 30-minute history of change of mental status. The patient had just climbed stairs when he first developed a headache that has become progressive; it is associated with nausea, non-bilious vomiting, and unilateral upper and lower extremity numbness. His physical exam reveals an alert patient who is not oriented to time, place, or person. He is afebrile, with a blood pressure of 185/108 mm Hg, and there is nuchal rigidity present. His neurological exam notes contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, and miosis. A CT scan without contrast was performed, and it is shown in the image below. Which of the following medications would be most appropriate for this patient? a. Nicardipine b. Heparin c. Methotrexate d. Dobutamine

d

A 72-year-old woman presents for management of an ischemic stroke. She reports difficulty seeing objects on her right side. You perform confrontational visual field testing as part of your neurological examination, and you discover she has a right inferior homonymous quadrantanopsia. This lesion localizes to what part of the body? a. Left optic tract b. Optic chiasm c. Right optic tract d. Left parietal lobe

Glasgow Coma Scale (GCS)

A scoring system used to describe the level of consciousness in a person following a traumatic brain injury Categories: Eye opening Motor Verbal Lowest possible score in each category is 1 Total lowest possible score is 3

b

An 18-year-old college freshman living in a dormitory presents with fever and chills, intense headache, vomiting, and stiff neck. His temperature is 39.2°C and pulse 140/min. After examination, the clinical diagnosis of meningitis is made. Lumbar puncture reveals fluid that is turbid and with elevated opening pressure. The cerebrospinal fluid (CSF) and blood are sent for microbiological studies. The patient is placed on intravenous Ceftriaxone. Gram stain of smears made from centrifuged CSF show many polymorphonuclear leukocytes (neutrophils)and intracellular gram-negative diplococci. A culture of CSF is sent and the results subsequently reveal Neisseria meningitidis group B. Based on this information, which of the following prophylactic interventions should be provided for the other dormitory residents? a. Chemoprophylaxis with Vancomycin b. Chemoprophylaxis with Rifampin c. Administration of tetravalent meningococcal polysaccharide vaccine d. Chemoprophylaxis with oral Penicillin

Infarct Core

Beyond repair of brain tissue by thrombolytic therapy

CN IV (Trochlear) Palsy

CN Palsies Etiology: MC congenital, trauma, microvascular disease, idiopathic Presentation: vertical diplopia, torsional diplopia, extorsion, head tilt, ipsilateral hypertropia (elevation of affected eye) Nonisolated palsies: Midbrain nuclear or fascicular lesions (eg, tumor, stroke, demyelination) is typically accompanied by other brainstem symptoms, such as hemisensory loss, hemiparesis, a central Horner syndrome, or other brainstem cranial neuropathies. Lesions of the subarachnoid space (eg, meningitis) are typically associated with other signs and symptoms including headache, stiff neck, and other cranial nerve abnormalities. Focal lesions (aneurysms, schwannomas) may produce isolated fourth nerve palsies. Cavernous sinus lesions are usually associated with other localizing signs (eg, third, fifth, or sixth nerve dysfunction, or Horner syndrome). Orbital apex lesions often involve third, fifth, and sixth cranial nerves as well as the optic nerve. Orbital involvement may also produce such signs as proptosis, chemosis, and orbital or conjunctival edema Dx: Unilateral-Parks-Bielschowsky 3 step test Which is the higher eye? Is the hypertropia worse in the right or left gaze? Is the hypertropia worse in right or left head tilt? Bilateral- alternating hypertropia on horizontal gaze, positive head tilt test to either shoulder, excyclotorsion >10 degrees, V pattern esotropia, underaction of both superior oblique muscles and/or overaction of both inferior oblique muscles, relatively small hypertropia in primary position Tx: treat underlying cause, prism therapy, patching one eye, botox

CN III (Oculomotor) Palsy

CN Palsies Etiology: structural lesions, cerebrovascular disease, inflammatory or infectious conditions, trauma, intracranial aneurysm (most feared cause, associated with SAH), ischemia (aka diabetic third nerve palsy, MC cause in adults), migraine Presentation: ptosis, paralysis of adduction, elevation, and depression of the eye, pain, binocular horizontal, vertical, or oblique diplopia, headache Complete internal dysfunction→ large unreactive pupil Partial internal dysfunction→ anisocoria (unequal pupil size) with sluggish but reactive pupil Dx: noncontrast CT (r/o SAH), MRI with MRA or CTA, LP Tx: observation for isolated palsies with complete external dysfunction and normal internal function, most deficits recover over weeks to months, patching one eye to alleviate diplopia, prism therapy, strabismus therapy, ptosis surgery

CN VI (Abducens) Palsy

CN Palsies Etiology: tumors, trauma, increased ICP, congenital Presentation: binocular horizontal diplopia that worsens with gaze to the paretic lateral rectus muscle, esotropia worse in gaze toward the paretic muscle (lateral incomitance) and an ipsilateral abduction deficit, eye pain Dx: MRI with and wo contrast Tx: most recover spontaneously, patching, prism therapy, strabismus surgery, botox

CN VII (Facial) Palsy (Bell's Palsy)

CN Palsies RF: pregnancy (3rd trimester, 1st week postpartum) Etiology: HSV, Herpes zoster, otitis media, lyme disease, guillain-barre, HIV, sarcoidosis, sjogren syndrome, tumors, stroke, melkersson-rosenthal syndrome Presentation: sudden onset unilateral facial paralysis, eyebrow sagging, inability to close eye, disappearance of nasolabial fold, mouth drawn to unaffected side, decreased tearing, hyperacusis, loss of taste sensation on anterior ⅔ tongue Dx: There is a diffuse facial nerve involvement manifested by paralysis of the facial muscles, with or without loss of taste on the anterior two-thirds of the tongue or altered secretion of the lacrimal and salivary glands Onset is acute, over a day or two; the course is progressive, reaching maximal clinical weakness/paralysis within three weeks or less from the first day of visible weakness; and recovery or some degree of function is present within six months CT, MRI Tx: eye protection, oral prednisone 60-80 mg x7 days, prednisone + valacyclovir 1000 mg TID for severe, botox for incomplete recovery

Traumatic Brain Injury

Closed Head Injuries Disruption in the normal function of brain Etiology: injury from bump, blow, or jolt to head, penetrating head injury (from bullet, shattered piece of skull) VIA —> fall, MVA, violence, sports injury, explosive blasts RF: kids, young adults (15-24), adults >60, males Mild= affects brain cells temporarily VS. Severe= bruising, torn tissues, bleeding, or death Presentation: Mild: LOC or dazed/confused, h/a, n/v, fatigue, speech problems, sleep problems, loss of balance/dizziness, light/sound sensitivity, mood swings, depression/anxiety, memory and concentration problems Mod/Severe: LOC w/in mins-hours, worsening h/a, repeated n/v, seizures, dilated pupils, insomnia, weakness/numbness in fingers and toes, nasal or aural drainage, profound confusion, slurred speech, agitation, coma CHILDS: change in eating and sleep, easy irritability, sad, loss of interest, drowsy, seizure Complications: altered consciousness (coma, negative state, brain death), seizure, vertigo, hydrocephalus, infection, BV damage, h/a, CN damage, intellectual/functional/cognitive inabilities, emotional/social/behavioral changes Dx: Glasgow Coma Scale (assess LOC after trauma, total score = 15, <8 = coma), CT, MRI Tx: Mild- rest, monitor, Mod-Sev- monitor in ER or ICU (O2, blood, BP), Meds (diuretics, anti-seizure, coma inducing drugs), surgery, rehab

Concussion

Closed Head Injuries Etiology: Caused by blow to head or penetrating head injury RF: contact sports or activities, MVA, assaults Most patients have a good prognterm-18osis, those who had concussions in the past have a longer recovery Presentation: Think/remembering problems, difficulty thinking clearly, feeling slowed down, difficulty concentrating, difficulty remembering new info, emotional/mood changes- irritability, sadness, More emotional, nervousness/anxiety, sleep disturbances- sleeping more or less than usual, trouble falling asleep, headaches, fuzzy/blurry vision, N/V, dizziness, sensitivity to light/noise, balance problems, feeling fatigued Mild: brief change in mental status or consciousness (MC) Severe: extended period of unconsciousness or memory loss Dx: CT scan is study of choice, MRI for prolonged symptoms or worsening symptoms Tx: cognitive & physical rest, may resume strenuous activity after resolution of symptom

Mild

Glasgow Coma Scale Severity 13-15

Severe

Glasgow Coma Scale Severity 3-8

Moderate

Glasgow Coma Scale Severity 9-12

Acute Toxic-Metabolic Encephalopathy

Encephalopathic Disorders Acute condition of global cerebral dysfunction in the absence of primary structural brain disease Etiologies: cerebral edema, drugs, electrolyte imbalances (hyper/hyponatremia), nutritional disorders, exogenous toxins Septic encephalopathy: MC cause EEG usually diffusely slow, may be triphasic waves and burst-suppression pattern, diffuse muscle weakness Tx by controlling underlying infection Presentation: delirium, agitated confusion or somnolence, impaired attention, tremor, myoclonus, asterixis, posturing and impaired brainstem reflexes in severe Dx: dx of exclusion, r/o alcohol withdrawal, meningitis, encephalitis, brain tumors, nonconvulsive seizures, central venous thrombophlebitis, bacterial endocarditis, fat embolism, basilar artery thrombosis, trauma, right hemisphere stroke CBC, coagulations, electrolytes (Ca, Mg, P, glucose, BUN, Cr, LFTs, ammonia, serum osmolality, ABGs), toxicology, blood and CSF cultures CT or MRI EEG Tx: treat underlying cause, discontinue CNS toxic meds, thiamine for ETOH, malnutrition, cancer, hyperemesis, or renal failure

Hepatic Encephalopathy

Encephalopathic Disorders Etiology: acute liver failure, medications, cirrhosis Presentation: cognitive deficits, impaired attention, reaction time, and memory, hepatic coma, bradykinesia, hyperreflexia, rigidity, myoclonus, asterixis, insomnia or hypersomnia Dx: psychometric testing, CT of brain, serum labs, ammonia concentrations, serum AFP Tx: lactulose, lactitol, or rifaximin to decrease ammonia levels, general supportive care, no dietary restriction

Uremic Encephalopathy

Encephalopathic Disorders Etiology: advanced renal failure Presentation: lethargy, irritability, disorientation, hallucinations, rambling speech, mild diffuse weakness, unsteady movements, tremor, myoclonus, asterixis, tetany Dx: EEG (prominent slow waves, intermittent frontal rhythmic theta activity, paroxysmal bilateral high-voltage delta waves, triphasic waves in frontal regions), neuroimaging Tx: dialysis

Hypoxic-Ischemic Encephalopathy

Encephalopathic Disorders Etiology: hypoxia or ischemia due to cardiac arrest, etc Presentation: amnesia, coma, cortical blindness, myoclonus, seizures, cerebellar ataxia, akinetic-rigid syndromes, bilateral arm weakness

Wernicke Encephalopathy

Encephalopathic Disorders Etiology: thiamine deficiency due to alcohol abuse, malnutrition, poor dietary intake, increased metabolic requirement, dialysis Pathophysiology: produces petechial hemorrhagic necrosis in midline brain structures Presentation: classic triad- encephalopathy (profound disorientation, indifference, and inattentiveness), oculomotor dysfunction (nystagmus, lateral rectus palsy, conjugate gaze palsies), gait ataxia, evidence of malnutrition, vestibular dysfunction, peripheral neuropathy, hypothermia Dx: no one lab to dx, EKTA, CT or MRI may show abnormalities, 2 of 4 Caine criteria: Dietary deficiency Oculomotor abnormalities Cerebellar dysfunction Either altered mental status or mild memory impairment Tx: administer thimine 500 mg IV over 20 mins TID for 2 days, 250 mg IV or IM QD for an additional 5 days, multivitamins

Hyperdense Artery Sign

Finding on CT that represents direct visualization of the clot within the lumen of the occluded artery Relies on hyperdense clot Depends on age of embolism Can be confirmed via CTA

Migraines

Headaches RF: Women, Ages 30-40, genetic, stress, dehydration, weather, sleep disturbances, hormones in women, not eating Presentation: two types With Aura (Classic Migraine): Prodrome: Yawning, euphoria, depression, irritability, food cravings, neck stiffness, constipation Aura: Visual: loss of vision, bright spots, expands as aura develops Sensory aura: tingling in one limb or side of face, followed by numbness, slow spread of symptoms Language & motor auras Auras without headache Headache: often unilateral, throbbing/pulsatile, N/V, photophobia, phonophobia Postdrome: Fatigue or exhaustion, mild elation or euphoria Without Aura: MC type Prodrome: Yawning, euphoria, depression, irritability, food cravings, neck stiffness, constipation Headache: often unilateral, throbbing/pulsatile, N/V, photophobia, phonophobia Postdrome: Fatigue or exhaustion, mild elation or euphoria Chronic Migraine: Headache occurring 15 or more days a month for more than 3 months, with the qualities of a migraine for at least 8 days a month Tx: NSAIDS, triptans, Sumatriptan + Naproxen, antiemetics/dopamine receptor antagonists (Chlorpromazine, Prochlorperazine, Metoclopramide) Preventative: Beta blockers, Amitriptyline & venlafaxine, Valproate & topiramate, Verapamil & flunarizine

Tension Headaches

Headaches RF: Women, caucasians, stress and mental tension Presentation: Mild-moderate intensity, bilateral , non-throbbing, dull, pressure, head fullness, pericranial muscle tenderness Tx: NSAIDs or aspirin, Caffeine + APAP, ASA, or NSAIDs Preventative: Amitriptyline

Cluster Headaches

Headaches Risk Factors: males, genetics Presentation: Severe orbital, supraorbital, or temporal pain, autonomic symptoms ipsilateral to the pain (ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, nasal congestion), short lived: 15-180 minutes, strictly unilateral, circadian periodicity Tx: Oxygen, Triptans* (Sumatriptan, Zolmitriptan (intranasal)) Preventative: CCBs (Verapamil), Glucocorticoids (Prednisone)

3 hours

How long is the optimal window for fibrinolytic therapy in acute stroke?

Meningitis

Infectious Disorders Etiology: bacteria (usually) within the subarachnoid space causing inflammation, typically spread by respiratory droplet or mucosa-to-mucosa spread, mortality is organism dependent (s. pneumonia is the worst), bacterial vs aseptic (viral, fungal, tb - not caused by a bacteria) Bacterial Causes: Meningococcus (N. meningitidis): gm- diplococci, associated w previous viral infections, common in dorms/military barracks, associated with meningococcemia, purpura fulminans, DIC, and septic shock, Tx Ceftriaxone Pneumococcus (S. pneumo): gm+ cocci, MC cause of bacterial, highest mortality, Tx Ceftriaxone + Vanco H. flu + E. coli: gm - bacilli, tx Ceftriaxone Listeria: gm+ bacilli, often food borne from unpasteurized dairy, contaminated meat/veggies/dairy, Tx Ampicillin +/- Gentamicin TB: chronic/subacute, CSF AFB low yield, PCR Aseptic Causes: Viral MC Enteroviruses Coxsackie b, echovirus: late summer/early autumn Lympho Choriomeningitis virus (LCM): rodent exposure Mumps virus EBV/CMV/VZV, HIV, HSV HSV: caused by HSV 2, MRI shows temporal lobe findings, presets with seizures and focal abnormalities, tx with Acyclovir IV x 4 weeks Fungal: Cryptococcus: immunocompromised patients, insidious onset, India ink stain or CSF cryptococcal antigen, Tx Amp B + Flucytosine, then fluconazole Presentation: fever (or hypothermia), headache, nuchal rigidity, altered mental status, photophobia, nausea/vomiting, kernig's sign (patient flexes neck as you flex patient's hip and extend knee), brudzinski's sign (patient flexes knee and hip as you flex the neck) Dx: standard orders: cbc, blood cultures, lumbar puncture, CT head Tx: do not delay treatment for lumbar puncture, if clinically suspected bacterial meningitis, must treat asap, empiric treatment: ceftriaxone (or pen g) + vancomycin + steroid, add ampicillin if listeria is plausible (infants, elderly, immunocompromised), add acyclovir if hsv is suspected, isolation (droplet), as csf comes back, alter therapy If not bacterial, d/c antibiotics, you were wrong! Gram+ cocci in pairs/chains, likely pneumococcus --> ceftriaxone and vancomycin and wait for sensitivity Gram- diplococci, likely meningococcus --> ceftriaxone alone Gram+ bacilli, likely listeria--> continue ampicillin, now consider adding gentamicin Gram- bacilli, either h. flu or e. coli --> ceftriaxone alone If hsv pcr +, acyclovir! If fungal +, id consult! If afb +, id consult!

Encephalitis

Infectious Disorders Etiology: usually viral- HSV 1, EBV, VZV, CMV, mumps, rabies, WNV, can also be arthropod-borne viruses (St. Louis virus, La Crosse virus, eastern or western equine) Lyme: tick borne, presents with EM, monoarticular arthritis, heart block, bell's palsy, false IgM testing, need CSF Borrelia, Tx with IV Ceftriaxone HIV/AIDS: Toxoplasma if not on Bactrim, ring enhancing lesion on CT, Tx with Pyrimethamine + Sulfadiazine + Leucovorin Presentation: fever, ams, focal deficits, seizures - csf similar to viral meningitis Dx: CT, MRI, CSF analysis w viral culture & PCR CSF: lymphocytes→ viral, RBCs in the absence of traumatic tap→ HSV or other necrotizing viral etiologies Tx: supportive care unless hsv, or next page, antipyretics, iv fluids, seizure prophylaxis, airway protection, monitor brain swelling/neuro checks

Viral

Infectious Disorders: Meningitis Total WBCs: <1000 Diff: lymphocytes Protein: mod increase Glucose: normal Lactate: normal

TB

Infectious Disorders: Meningitis Total WBCs: <500 Diff: lymphoctes & monocytes Protein: mod/marked increase Glucose: decrease Lactate: increase

Fungal

Infectious Disorders: Meningitis Total WBCs: <500 Diff: lymphoctes & monocytes Protein: mod/marked increase Glucose: normal/decrease Lactate: increase

Bacterial

Infectious Disorders: Meningitis Total WBCs: >1000 Diff: neutrophils Protein: marked increase Glucose: marked decrease Lactate: marked increase

Essential Tremor

Movement Disorders Pathophysiology & Epidemiology: Idiopathic Family history 30-70% of cases, first degree relatives higher risk, no genetic identifiers Most common cause of postural/action tremor 5% worldwide Presentation: Tremor- Bilateral > unilateral Hands, arms: + Head (yes or no movements) - if alone, dystonia +Voice Legs unusual - more likely parkinsonism Increases in amplitude: See with arms extended Exacerbated with finger-nose-finger at very end, bringing liquids to mouth Stress, caffeine Decreases: Rest, alcohol USUALLY no rigidity, gait abnormalities or other neuro sx * Older patients may have bradykinesia and mild cogwheel rigidity* Dx: Clinical, rule out other causes- Wilson's disease: Ceruloplasmin, serum copper, Environmental: Heavy metals screen - lead, Parkinson's: PET scan/DaTscan - consider if changing course or considering surgery (DBS) Tx: Indicated when symptoms cause impairment, as needed or continuous Monotherapy or combination: Propranolol, Primidone, Alprazolam (prn), Gabapentin, Topiramate, Nimodipine Surgery: DBT, Thalamotomy (MRI focused ultrasound), Botox (head/voice)

Huntington Disease

Movement Disorders Pathophysiology & Epidemiology: neurodegenerative disorder Abnormal CAG repeats causing abnormal huntingtin protein --> death of neuron, basal ganglia often affected Autosomal dominant, usually presents later in life, may have already had children! Worldwide prevalence 2.7 per 100,000, 5-8 per 100,000 in Europe and North America, lower prevalence in other ethnicities Presentation: Chorea: involuntary, rapid, non-repetitive movement, face, arm, trunk, legs Restlessness --> More obvious movements, interferes, patient not bothered by movement Parakinesia - incorporate abnormal movements into purposeful movements Hypotonia, hyperreflexia, dystonia (ie. hands while walking), mild bradykinesia Dysarthria, dysphagia, involuntary vocalization Psychiatric illness (can be before chorea): Poor social relationships, Irritable, depression, suicidal, psychosis: paranoia, delusions, hallucinations Dementia: executive dysfunction, impaired judgement, cannot multitask, impulsive, lack of insight to symptoms, later finding Dx: Genetic testing with genetic counselor, CAD repetition in HTT gene, imaging not warranted for diagnosing HD, MRI ?changes in basal ganglia, may help to rule out structural lesions (MS, CJD, neoplasm) Tx: Multidisciplinary team, Tetrabenazine (increased suicide ideation), BZD, SSRI, typical/atypical antisychotics, Medical marijuana, support groups

Parkinson Disease

Movement Disorders Pathophysiology: ↓ Dopamine in STN→ ↑ Inhibitory from GPi and SN, ↓ messages to thalamus and motor cortex= ↑ Motor symptoms (bradykinesia) Development of inclusion bodies in SNr = Lewy Bodies Other non-dopaminergic/non-motor effects: Serotonin receptors in brainstem Olfactory system Cerebral hemispheres Spinal cord Peripheral autonomic nervous system Etiology: Sporadic (85-90%) OR Familial/genetic (10-15%) RF: Genetic factors - onset <40-50, Parkin gene - recessive, Alpha-synuclein gene - dominant, ?Environmental factors - onset >50, pesticides, rural living, drinking well water, ↓ Risk smoking and caffeine Epidemiology: 2nd most common neurodegenerative disorder, (Alzheimer's is 1st), ~1 million in US and ~5 million worldwide, Average age of onset = 60 years old, as young as 20 years old (familial), 10-15% of PD patients <50 years old Presentation: Unilateral symptoms with resting tremor, bradykinesia, rigidity (postural instability not unilateral), micrographia: small handwriting, masked faces: lack of smile, reduced eye blink: "reptilian stare", stooped posture: simian posture, soft voice: hypophonia, dysphagia, freezing, anosmia, sensory disturbances (pain), mood disorder (depression), sleep disturbance (Non-REM disorders), acting out dreams, violent, orthostatic hypotension, gastrointestinal disturbances, genitourinal disturbances, sexual dysfunction, cognitive impairment/dementia Physical Exam: Vitals: Orthostatic BP General appearance: Masked facies, seborrhea, oily skin, lack of arm movements with conversation Neurologic: MMSE/MoCA, PHQ-9, hyposmia (UPSIT), slowed saccades, decreased vertical gaze (PSP), cogwheel rigidity, asym DTR/Babinski, vascular parkinsonism from prior stroke, MSA, ↓ Rapid finger/foot tapping, slow/skip beat Resting tremor: Watch without them knowing while seated and walking Finger-nose-finger improved tremor Micrographic, spiral test Gait testing: Rise from chair without using arms, start of movement, reduced arm swing, pill rolling tremor, shuffle, en bloc turns (3-5+ turns), propulsion or retropulsion Dx: Clinical, response to Levodopa, PET/SPECT scans: helpful for difficult cases, ↓ uptake of striatal dopaminergic markers genetic testing (research only), parkin gene mutations - onset <40 years old Tx: Levodopa, dopamine agonist, MAO-B Inhibitor, Amantadin, Anticholinergics, COMT inhibitors, device-assisted/surgical procedures Lifestyle Modifications: Education: Patient, caregiver, spouse, children Support groups - local Parkinson's Foundation, Dent Neurologic, BGH Exercise: May slow down rigidity, flexed posture, improves physical and mental wellbeing, Tai chi, brisk walking, swimming, water aerobics Physical and occupational therapy Music therapy Speech therapy: Help with hypophonia, dysarthria Nutrition: High fiber, hydration (constipation), avoid high fat meals (interferes with med absorption) Palliative care

Tourette Disorder

Movement Disorders RF: onset usually childhood (2-5 yo), usually associated with obsession compulsions, ADHD Etiology: genetic, SLITRK1 and HDC gene Presentation: motor tics of face, head, and neck (blinking, shrugging, head thrusting, sniffling), verbal/phonetic tics (grunting, throat clearing, obscene words-coprolalia, repetitive phrases, echolalia), self-mutilating Dx: clinical features with onset before age 21 Tx: habit reversal tx, Tetrabenazine, dopamine blocking agents (Haloperidol, Risperidone), alpha-adrenergics (clonidine, guanfacine)

Minor

NIHSS Severity 1-4

Moderate/Severe

NIHSS Severity 16-20

Severe

NIHSS Severity 21+

Moderate

NIHSS Severity 5-15

Multiple Sclerosis

Neuromuscular Disorders Pathophysiology: An autoimmune disease wherein the body makes antibodies against the myelin basic protein which destroys the myelin sheath, results in poor transmission of signal along central nerves, primarily upper motor neuron disease (brain & spinal cord) Etiology: Causes unknown, messages that travel along that nerve may be slowed or blocked, nerve may also become damaged itself, vitamin D deficiency? RF: Age 15-60, women, family Hx, viral infections (EBV), caucasians (but Native Americans and African Americans are affected much worse), temperate climates (Vitamin D?) Presentation: Numbness or weakness in one or more limbs that typically occurs on one side of the body at a time, or the legs and trunk; tingling and pain, partial or complete loss of vision, usually in one eye at a time; Prolonged double vision (one and a half syndrome), electric-shock sensations that occur with certain neck movements, especially bending the neck forward (Lhermitte sign), tremor, lack of coordination or unsteady gait, slurred speech, fatigue, dizziness Dx: physical exam, LP demonstrates oligoclonal bands, MRI 4 Types: Relapsing-Remitting: most common form of multiple sclerosis, have temporary periods called relapses, flare-ups or exacerbations, when new symptoms appear Secondary-Progressive: symptoms worsen more steadily over time, with or without the occurrence of relapses and remissions, most people who are diagnosed with RRMS will transition to this at some point Primary-Progressive: not very common, characterized by slowly worsening symptoms from the beginning, with no relapses or remissions Progressive-Relapsing: rare, characterized by steadily worsening disease from beginning, with acute relapses but no remissions, with or without recovery Tx: Aimed at Relapsing-Remitting form, corticosteroids, plasma exchange (plasmapheresis), immunotherapies

Myasthenia Gravis

Neuromuscular Disorders Pathophysiology: inefficient skeletal mm neuromuscular transmission due to autoimmune Ab against acetylcholine (nicotinic) postsynaptic receptor at neuromuscular joints (decreased ACh receptors)--> progressive weakness with repeated muscle use & recovery with periods of rest Etiology: autoimmune disorder of peripheral nerves, MC have thymic abnormality (hyperplasia or thymoma) RF: MC in young women, HLA-DR3, may occur postpartum Presentation: Ocular weakness: usually presents first and more severe, extraocular mm weakness→ diplopia, ptosis, pupils spared Generalized muscle weakness: least in morning, worsened with repeated muscle use throughout day (relieved with rest), fluctuating Bulbar (oropharyngeal mm weakness): weakness with prolonged chewing, dysphagia Respiratory mm weakness: respiratory weakness→ respiratory failure=myasthenic crisis Normal sensation & reflexes Dx: Tensilon test (rapid response to IV edrophonium), + ACh antibodies, + muscle specific tyrosine kinase Ab, ice pack test (improves with cold) Tx: ACh inhibitors (pyridostigmine, neostigmine), immunosuppression with steroids, azathioprine, or cyclosporine, plasmapheresis or IVIG use in MG crisis, thymectomy if thymoma, avoid quinolones or aminoglycosides

Guillain-Barre Syndrome

Peripheral Nerve Disorders AKA Acute inflammatory demyelinating polyneuropathy (AIDP) NEUROLOGIC EMERGENCY 1-4 per 100,000 people Idiopathic autoimmune response Demyelination injury to motor and sensory nerves (+/- axonal) RF: Young adult - early middle age adult > children, males > Females, recent URI/GI illness (Campylobacter jejuni), recent immunizations (influenza vaccine) Presentation: Distal symmetric weakness and numbness that RAPIDLY travels proximally with autonomic instability, respiratory depression, lasts 3-4 weeks, profound weakness/paralysis, global areflexia, decreased sensation distal 🡪 proximally Dx: CSF protein elevated (>400), NORMAL CELL # (usually), may need repeat LPs to see rising protein - delay in 1-2wk, EMG/NCS for prognosis, nerve biopsy, PFTs Tx: Hospital/ICU, plasmapheresis QOD x 3-5 days +/- 5 days of IVIG (0.4g/kg/d), +/- Ventilation support, PT/OT Prognosis: Good once recognized and treatment started, rarely recurs

Complex Regional Pain Syndrome

Peripheral Nerve Disorders AKA Reflex sympathetic dystrophy Unknown pathogenesis ?Inflammatory markers, autonomic system RF: Tissue trauma of limb, fractures, crush injury, sprain, surgery Presentation: Pain (Burning, stinging, deep - continuous), not confined to particular nerve pattern (may start at one area then spread), motor weakness, atrophy, contracture with chronic sx, allodynia (non painful stimuli now painful), hyperpathia (painful stimuli creates exaggerated pain response), vasomotor dysfunction (skin coloration), temperature change (change in blood flow), focal edema, increased sweating, connective tissue changes, increased hair growth, decreased nail growth, skin atrophy Stages: Weeks-months: PAIN, sensitivity, autonomic 3 - 6 Months: Edema, thickening skin, muscle wasting > 6 Months: Contractures, waxy thickened skin, brittle nails Dx: Diagnosis of exclusion, r/o infection, compartment syndrome, PVD, DVT, Neuropathy, thoracic outlet syndrome, autoimmune, conversion, factitious Tx: PT/steroids in early stages, counseling, NSAIDs, antidepressants, anticonvulsants, bisphosphonates, Calcitonin, CCB, topical lidocaine, capsaicin, nerve blocks

Peripheral Neuropathy

Peripheral Nerve Disorders Occurs when there is a lesion in a peripheral nerve Causes weakness- Is more prominent distally at onset, Asymmetric typically Presents w/ decreased DTR Sensory changes- numbness, tingling, paresthesias Muscle atrophy, fasciculations Causes: Diabetes, trauma, entrapment, vasculitis, hypothyroidism, vitamin deficiencies

Hypothyroidism Peripheral Neuropathy

Peripheral Nerve Disorders: Peripheral Neuropathy Causes carpal tunnel syndrome (type of peripheral neuropathy) Uncommon cause of peripheral neuropathy Can occur due to severe, long-term untreated hypothyroidism May result due to hypothyroidism causing fluid retention resulting in swollen tissues which exert pressure on nerves Presentation: pain, burning sensation, numbness, & tingling, can progress to muscle weakness or loss of muscle control Tx: Treat w/ levothyroxine

Diabetic Peripheral Neuropathy

Peripheral Nerve Disorders: Peripheral Neuropathy Is a complication of DM, Distal symmetric neuropathy Presentation: "stocking/glove" pattern of decreased proprioception, paresthesias, & pain, typically begins in feet and later moves to hands, affects longer nerves 1st, decreased DTR, sensation loss leads to: Ulcer formation, Charcot's Joints Tx: Gabapentin, TCA's, Lyrica

Vitamin B12 Deficiency Peripheral Neuropathy

Peripheral Nerve Disorders: Peripheral Neuropathy Main dietary sources: fish & meat, Stored in liver for up to 3 or more years, Bound to intrinsic factor- is absorbed by the terminal ileum Etiologies: pernicious anemia- lack of intrinsic factor, most common cause, gastrectomy, Poor diet (vegetarian, alcoholic), Crohn's Disease Presentation: peripheral neuropathy, paresthesias especially in lower extremities, Loss of position & vibratory sensation, Can distinguish B12 deficiency from folate deficiency, spinal cord demyelination, ataxia, weakness, decreased DTR, abnormal Babinski, macrocytic anemia, stomatitis & glossitis Dx: Peripheral smear- Increased MCV, Hypersegmented neutrophils Tx: IM B12 (cyanocobalamin) q monthly

Mean Arterial Pressure

Pressure forcing blood into tissues, averaged over cardiac cycle Measured by calculating [systolic BP + (2*diastolic BP)]/3 Normal is typically 70-100 mmHg

Focal (Partial) Seizures

Seizure Disorders Arise at a specific locus of the cerebral cortex RF: adults, >18 yo Etiologies: Acquired: temporal-lobe epilepsy most common Idiopathic: generally age-related Presentation: Severity can range from disorder of sensation to generalized convulsion Types: simple, complex, secondarily generalized Simple: Consciousness remains intact, may be motor, sensory, autonomic or psychic Complex: Consciousness is impaired; most common type of seizure in adults, 85% epileptogenic focus is in the temporal lobe, 15%: usually frontal lobe Purposeless, involuntary, repetitive movements Ex: smacking lips, chewing, patting, walking May become aggressive if restraint is attempted Auras: Sensory, autonomic, motor sxs patient is aware of that precede or accompany seizure Secondarily Generalized (Tonic-Clonic): Focal neuronal burst spreads to the remaining brain Dx: focal EEG changes Simple: focal discharge Complex: interictal spikes with slow waves in temporal area Tx: phenytoin + carbamazepine

Status Epilepticus

Seizure Disorders Continuous seizure activity persisting greater than 15 minutes (30 minutes) or two or more episodes occurring in 30 minutes without full recovery between seizures Presentation: Generalized convulsive: repeated motor convulsions w/o recovery Nonconvulsive: 'epileptic twilight": continuous Simple partial: repeated focal motor seizures or focal impairment of function (aphasia) without LOC Prognosis: mortality 30% Tx: ABCs, blood pressure monitoring, IV, oxygenation, temp

Seizures

Seizure Disorders Etiologies: trauma (only treated with Dilantin or Depakote), medications or withdrawal, ischemia, hypoglycemia, hyponatremia, hypocalcemia, hepatic encephalopathy, porphyria, eclampsia (TOC is magnesium sulfate), hyperthermia, uremia, febrile seizures Dx: Assess vital functions, oral airway, Oxygen, establish IV infusion with normal saline, monitor temp and blood pressure, draw blood for electrolytes, glucose, AED levels, CBC, BUN and SGOT Tx: Administer thiamine and 50 ml of 50% glucose IV push, Lorazepam (or diazepam), Start phenytoin IV infusion (slow rate), Monitor BP for hypotension and ECG, If refractory, phenobarb by endotracheal tube, If still refractory: barb coma: monitor by EEG Valproic acid has broadest anti-epileptic activity All AEDs are teratogenic, begin folic acid supplementation 6 months before conception

Generalized Seizures

Seizure Disorders Generalized involvement of the brain; no focus Etiologies: Primary: No identifiable etiology, genetic factors predominate, includes absence seizures Secondary: Due to acquired cerebral diseases, seizures often drug-resistant, includes Lennox-Gastaut Syndrome of childhood Lennox-Gastaut Syndrome: Collection of seizure types which are usually intractable. Often associated with perinatal insult. Presentation: Consciousness is usually lost, infrequent aura Subtypes: Absence (petit mal): RF: Always begin in childhood, end by age 20, spells can be induced by hyperventilation Presentation: Brief loss of consciousness, minimal motor symptoms (eye-twitching), "stare into space," look like daydreaming, unaware of attack, no post-ictal state Dx: EEG- 3-Hz generalized spike-wave discharges, must be differentiated from complex partial seizures Myoclonic: Brief jerking movement, localized or generalized, associated mainly with rare neurologic conditions, anoxia Clonic: Rhythmic twitching of the body, associated with LOC Tonic: Brief attacks of stiffness, may be localized or generalized, can involve respiratory movements, generally associated with LOC Atonic: Loss of posture ('drop attack') Tonic-clonic (grand mal): Bilateral symmetric seizure without focal onset, begins with sudden loss of consciousness Tonic Phase: Becomes rigid, Trunk & limb extension, Pt becomes apneic, Lasts about 60 seconds Clonic Phase: Repetitive, rhythmic jerking of limbs, Lasts for about 2-3 minutes Patient then becomes flaccid and comatose, eventually regaining consciousness Post-ictal phase: Confusion, Drowsiness, Can last for hour Other features: Tongue biting, Vomiting, Apnea, Incontinence of urine or feces Can have an aura prior Dx: CBC, electrolytes, blood glucose, LFTs, renal function tests, serum calcium, UA, EEG Absence: bilateral symmetric 3 Hz spike & wave action, or may be normal Tonic-clonic: generalized high amplitude, rapid spiking Tx: tonic-clonic or myoclonic- phenytoin + carbamazepine, absence- zarontin + valproic acid

Complex Partial

Seizure Disorders: Focal Seizures Consciousness is impaired; most common type of seizure in adults, 85% epileptogenic focus is in the temporal lobe, 15%: usually frontal lobe Purposeless, involuntary, repetitive movements Ex: smacking lips, chewing, patting, walking May become aggressive if restraint is attempted Auras: Sensory, autonomic, motor sxs patient is aware of that precede or accompany seizure Dx: interictal spikes with slow waves in temporal area on EEG

Simple Partial

Seizure Disorders: Focal Seizures Consciousness remains intact, may be motor, sensory, autonomic or psychic Dx: focal discharge on EEG

Secondarily Generalized

Seizure Disorders: Focal Seizures Focal neuronal burst spreads to the remaining brain

Tonic-Clonic (Grand mal) Seizures

Seizure Disorders: Generalized Seizures Bilateral symmetric seizure without focal onset, begins with sudden loss of consciousness Tonic Phase: Becomes rigid, Trunk & limb extension, Pt becomes apneic, Lasts about 60 seconds Clonic Phase: Repetitive, rhythmic jerking of limbs, Lasts for about 2-3 minutes Patient then becomes flaccid and comatose, eventually regaining consciousness Post-ictal phase: Confusion, Drowsiness, Can last for hour Other features: Tongue biting, Vomiting, Apnea, Incontinence of urine or feces Can have an aura prior

Tonic Seizures

Seizure Disorders: Generalized Seizures Brief attacks of stiffness, may be localized or generalized, can involve respiratory movements, generally associated with LOC

Inferior, Middle, or Anterior Cerebral TIA

Vascular Disorders: TIA Locations Cerebral hemisphere dysfunction. sudden HA, speech changes, confusion

Posterior Cerebral TIA

Vascular Disorders: TIA Locations Somatosensory dysfunction

AV Malformation

Vascular Disorders Abnormal tangle of BV connecting arteries and veins = disruption to nL blood flow and O2 circulation = arteries and veins weaken or rupture = rupture leads to hemorrhage, stroke, or brain damage Etiology: idiopathic or congenital Vein of Galen Defect- happens after birth, hydrocephalus = enlarged head, swollen veins in scalp, FTT, CHF, seizure RF: FHx, congenital conditions like HHT (hereditary hemorrhagic telangiectasia or Osler-Weber-Rendu syndrome) Presentation: bleeding, loss of neurologic function, h/a, n/v, seizure, LOC, dizziness, memory loss, weak muscles/paralysis, numbness/tingling, pain, hallucination Dx: cerebral angiography, CT, MRI, MRA, transcranial doppler US Tx: medications (symptomatic- seizure, h/a, back pain), surgery (endovascular embolization, stereotactic radiosurgery)

Cerebral Aneurysm

Vascular Disorders Ballooning of a blood vessel in the brain Can leak or rupture causing a hemorrhagic stroke Subarachnoid hemorrhage is most common complication Most aneurysms don't rupture Etiologies: Thinning of atrial walls RF: Elderly, women, smokers, HTN, atherosclerosis, drug abuse, head injury, alcohol consumption, blood infections, post-menopause Sx: Unruptured: May be asymptomatic, large aneurysms may cause symptoms, pain above/behind the eye, dilated pupil, change in vision/double vision, numbness, weakness, paralysis to one side of the face, drooping eyelid "Leaking" aneurysm: sudden, extreme HA, can lead to rupture Ruptured aneurysm: sudden, severe HA,"worst HA of their life", N/V, stiff neck, blurred vision, seizure, drooping lid, loss of consciousness, confusion Dx: CT 1st test done, LP with RBC's if ruptured, MRI/MRA, Cerebral Angiogram Tx: Surgery, clip or coil aneurysm, CCB, Anti-seizure meds

Intracranial Hemorrhage

Vascular Disorders Located intraparenchymal Caused by HTN- esp. in basal ganglia Accounts for 20% of strokes Mechanism: HTN, arterio-venous malformation, trauma, amyloid dz Sx: HA, N/V, may have loss of consciousness, hemiplegia, hemiparesis, is not associated w/ lucid intervals, sxs occur w/in minutes to hours and gradually increase in intensity Dx: CT scan, intraparenchymal bleed DO NOT perform an LP if suspect ICH! Causes mass effect and herniation of the brain!!! Tx: supportive, steroids, seizure prophylaxis, hematoma evacuation if mass effect

Transient Ischemic Attack (TIA)

Vascular Disorders Transient episode of neurological deficits caused by focal: brain, spinal cord, or retinal ischemia NO acute infarction Most resolve in 30-60 minutes Never last more than 24 hours MC due to embolus from carotids or vertebrobasilar 50% of pts w/ TIA will have a CVA w/in 24-48 hours Sx: Depends on where there is ischemia Internal Carotid: amaurosis fugax, temporary vision loss, weakness in contralateral hand Inferior, Middle, or Anterior Cerebral Artery: cerebral hemisphere dysfunction. sudden HA, speech changes, confusion Posterior Cerebral Artery: somatosensory dysfunction Vertebrobasilar: brainstem/ cerebellar dysfunction, gait & proprioception dysfunction Dx: CT scan to r/o hemorrhage, carotid doppler (look for stenosis), endarterectomy advised if stenosis 70-99%, CT angiography/MRA images cerebral vasculature for stenosis/occlusion Tx: ASA w/ dipyridamole or Plavix, thrombolytics are contraindicated, reduce risk factors: DM🡪 glucose control, HTN🡪 BP control, A Fib🡪 put on anticoagulation, increase physical activity

Syncope

Vascular Disorders Transient loss of consciousness/ postural tone secondary to acute decrease in cerebral blood flow, Characterized by rapid recovery of consciousness Etiology: Seizure disorder Cardiac: Sudden & w/o prodromal sxs, Due to: arrhythmias, obstruction of blood flow, massive MI Vasovagal syncope "Neurocardiogenic", Most common cause- up to 50%, age 40 Due to: stress, pain, fear, fatigue, claustrophobic situations, etc. Prodrome: pallor, diaphoresis, lightheadedness, nausea, diminished vision, roaring in ears Pathophysiology: Normally, standing up causes blood to pool lower extremities. This causes decreased CO, stroke volume, & BP. These changes are compensated for by increase in sympathetic tone- vasoconstriction & tachycardia In vasovagal syncope, the compensatory response is interrupted, there is withdrawal of sympathetic stimulation & enhanced parasympathetic activity, leads to bradycardia, vasodilation, decreased BO, & decreased cerebral perfusion Tx: assume supine position & elevating legs Orthostatic hypotension Can occur due to diabetes, older age, prolonged bed rest, and certain medications Has some overlap w/ vasovagal syncope Posture is main cause - Sudden standing or prolonged standing are precipitating causes Associated w/ prodrome sxs- lightheadedness, nausea, etc. Severe cerebrovascular disease- Rare cause of syncope Metabolic causes- hypoglycemia, hyperventilation Hypovolemia from hemorrhage Dx: 1st rule out life threatening conditions- MI, hemorrhage, arrhythmias, orthostatic vitals, obtain an EKG for all patients- May need Holter monitor, Tilt Table Test- Diagnose neurocardiogenic syncope, can also obtain CT, echo, etc.

Epidural Hematoma

Vascular Disorders: Hemorrhagic Stroke Arterial bleed Bleeds quickly Occurs between the skull & dura Most commonly occurs in temporal area Mechanism: Occurs after skull fracture, Fx in temporal bone= disrupts middle meningeal artery Sx: Brief LOC, have a period of lucidity, eventual HA, N/V, focal neuro deficits, rhinorrhea—CSF, coma Dx: CT, convex shaped bleed, doesn't cross suture line Tx: Need to evacuate early! Observe if small

Subarachnoid Hemorrhage

Vascular Disorders: Hemorrhagic Stroke Arterial bleed Occurs between the arachnoid & pia mater Mechanism: MC caused by Berry Aneurysm Rupture, MC occur @ Circle of Willis, Aterio-venous malformation Sx: Thunderclap sudden HA, "worse HA of my life, " may have brief LOC, N/V, meningeal Irritation, stiff neck, photophobia, delirium, NO focal neuro deficits Dx: CT scan 1st, If CT is negative & have a high suspicion do lumbar puncture (xanthochromia, increased CSF pressure) Tx: supportive, bed rest- no exertional activities, stool softeners, seizure prophylaxis, anti-anxiety meds, keep BP low

Subdural Hematoma

Vascular Disorders: Hemorrhagic Stroke Venous bleed, therefore, slower bleed Occurs between the dura & arachnoid mater Occurs due to tearing of bridging veins MC occurs in elderly Mechanism: Blunt trauma, often causes bleeding on the other side of the injury= "contre-coup" Sx: focal neuro deficits Dx: CT, concave- crescent shaped, can cross suture lines Tx: Evacuation if massive or 5mm midline shift, supportive

Basilar Artery Infarct

Vascular Disorders: Ischemic Stroke Locations Causes cerebellar dysfunction, CN palsies, decreased vision

Anterior Cerebral Artery Infarct

Vascular Disorders: Ischemic Stroke Locations 2% Sx: contralateral sensory/motor loss/paresis, greater in lower leg/foot compared to upper extremity, abnormal gait, face is spared w/ speech preservation, impaired judgement, confusion, personality changes, urinary incontinence, UMN weakness Dx: Non-contrast CT- r/o hemorrhage, CT scan can be normal during 1st 6-24 hours Tx: Thrombolytic therapy w/in 3 hours of onset

Vertebral Artery Infarct

Vascular Disorders: Ischemic Stroke Locations Causes vertigo, N/V, nystagmus, diplopia, ipsilateral ataxia Dx: CT scan, small punched out hypodense areas Tx: ASA, control HTN/DM/ other risk factors Good prognosis- resolve deficit in hours to 6 weeks

Middle Cerebral Artery Infarct

Vascular Disorders: Ischemic Stroke Locations MC- 70% Sx: contralateral sensory/motor loss/paresis, seen more in the face & arm compared to leg/foot, visual: contralateral homonymous, gaze preference towards SIDE OF LESION, Broca's or Wernicke's aphasia, agraphia, spatial defects, dysarthria, If involves face: will affect lower face, pts can still raise eyebrows! Dx: Non-contrast CT- r/o hemorrhage, CT scan can be normal during 1st 6-24 hours Tx: Thrombolytic therapy w/in 3 hours of onset

Posterior Cerebral Artery Infarct

Vascular Disorders: Ischemic Stroke Locations Sx: visual hallucinations, contralateral homonymous hemianopia, crossed sxs, ipsilateral CN deficits w/ contralateral muscle weakness, coma, drop attacks Dx: Noncontrast CT to r/o hemorrhage, CT can be normal for up to a day Tx: thrombolytic therapy w/in 3 hours of onset

Ischemic Stroke

Vascular Disorders: Stroke Most common type of stroke- 80% Causes: thrombotic, embolic, cerebrovascular occlusion, lacunar Infarct Small vessel dz due to occlusion of penetrating branches of cerebral arteries RF: HTN Sx: Pure motor sxs or pure sensory, hemiparesis, hemiplegia, ataxic hemiparesis, dysarthralgia Anterior Circulation: Middle Cerebral Artery Infarct MC- 70% Sx: contralateral sensory/motor loss/paresis, seen more in the face & arm compared to leg/foot, visual: contralateral homonymous, gaze preference towards SIDE OF LESION, Broca's or Wernicke's aphasia, agraphia, spatial defects, dysarthria, If involves face: will affect lower face, pts can still raise eyebrows! Dx: Non-contrast CT- r/o hemorrhage, CT scan can be normal during 1st 6-24 hours Tx: Thrombolytic therapy w/in 3 hours of onset Anterior Cerebral Artery 2% Sx: contralateral sensory/motor loss/paresis, greater in lower leg/foot compared to upper extremity, abnormal gait, face is spared w/ speech preservation, impaired judgement, confusion, personality changes, urinary incontinence, UMN weakness Dx: Non-contrast CT- r/o hemorrhage, CT scan can be normal during 1st 6-24 hours Tx: Thrombolytic therapy w/in 3 hours of onset Posterior Circulation: Posterior Cerebral Artery Sx: visual hallucinations, contralateral homonymous hemianopia, crossed sxs, ipsilateral CN deficits w/ contralateral muscle weakness, coma, drop attacks Dx: Noncontrast CT to r/o hemorrhage, CT can be normal for up to a day Tx: thrombolytic therapy w/in 3 hours of onset Basilar Artery: Causes cerebellar dysfunction, CN palsies, decreased vision Vertebral Artery: Causes vertigo, N/V, nystagmus, diplopia, ipsilateral ataxia Dx: CT scan, small punched out hypodense areas Tx: ASA, control HTN/DM/ other risk factors Good prognosis- resolve deficit in hours to 6 weeks

Internal Carotid TIA

Vascular Disorders: TIA Locations Amaurosis fugax, temporary vision loss, weakness in contralateral hand

Vertebrobasilar TIA

Vascular Disorders: TIA Locations Brainstem/ cerebellar dysfunction, gait & proprioception dysfunction

d

What condition is characterized by fine movements that are absent at rest, occur with activity, and worsen as the target is neared? a. Chorea b. Asterixis c. Postural tremor d. Intention tremor

Noncontrast CT

What is the test of choice for assessing an acute stroke?