Neuro Exam 2

Somatosensory pathways

(slide 6 pp) Start with neurons in skin, two systems in spinal cord (spinothalamic pain crosses to other side, medial leminscus light touch/proprioception/ vibration cross in medulla) and meet in thalamus Ventrolateral thalamus are cerebellar signs, ventroposteriorlateral thalamus relays the sensory info to somatosensory cortex and then goes to primary somatosensory cortex

Subarachnoid Hemorrhage Where, symptoms, most common cause, CSF, complications

-Bleeding on the outside of the brain in subarachnoid space, from arteries surrounding the brain -In this type of stroke, there is bleeding into the subarachnoid space so that the cerebrospinal fluid contains blood which is very irritating to the meninges. -The symptoms include the abrupt onset of the "worst headache of the patient's life", loss of consciousness, nausea and vomiting, and neck stiffness usually without focal neurologic findings. -The most common cause of subarachnoid hemorrhage (80%) is a cerebral aneurysm. These usually affect branching points in the vessels in the Circle of Willis (anterior communicating artery, middle cerebral bifurcation, posterior communicating, tip of basilar) and may be multiple. CT scan shows blood in the subarachnoid space in 95% of patients on the day of onset but this drops to 50% by one week. -A spinal fluid examination shows xanthochromia (CSF looks yellow because of blood breakdown products) for 2-3 weeks following the event. This is an important diagnosis to make because there is a 15-20% risk of rebleeding in the first two weeks after the first hemorrhage with a mortality rate of 60%. IF THERE is bleeding in subarachnoid space, blood gets into CSF and goes all over the body -The second major complication after rebleeding is the occurrence of vasospasm of the vessels in the Circle of Willis which leads to ischemic stroke and occurs 3-10 days after the hemorrhage. Cerebral angiography is done early in patients with subarachnoid hemorrhage to look for an aneurysm which is treated by placing a surgical clip across the neck or placing coils inside the aneurysm to cause it to clot. -The complication of ischemic stroke can be prevented by treating patients with medication (nimodipine, a calcium channel blocker) to prevent vasospasm.

Work-up of dementia

-Careful history -Complete mental status & neurological exam -Blood studies CBC, electrolytes, LFTs B12 folate levels, Thyroid function tests, VDRL, FTA, HIV -Lumbar puncture -EEG -MRI -PET

1. Evaluating cranial nerves and key functions All 12

1 Olfactory- smell 2 Optic- vision 3 occulomotor- eyeball 4 trochlear- eyeball 5 trigeminal - face sensation, mastication 6 abducens - eyeball 7 facial nerve- face movement 8 vestibulocochlear - hearing and equilibrium 9 glossopharyngeal- pharynx sensation (gag reflex) 10 vagus - pharynx movement (gag reflex) 11 Accessory nerve- spinal- turns head, shrugs shoulders, trapezius/sternocleidomastoid 12 hypoglossal- moves tongue

Neurological Examination 1- His vital signs were normal except for an irregular pulse. He was alert and oriented. His speech was slurred, but otherwise fluent, and comprehension was normal. pp 21

1- Irregular pulse is high risk of atrial fibrillation and blood clot to travel to brain or heart. Slurred speech but language seems to be normal, causes of this: damage to the motor systems important for pronouncing words. Guessing stroke in the person is on the right since left is responsible for the language, slide 1 on 4b: However Language areas are not only in the frontal lobes. In addition, we have: Wernicke's and sensory language area. Anatomy: -Wernicke's area corresponds to BA 22 (posterior 2/3 of superior temporal gyrus). -Many authors also include in Wernicke's area a rim of adjacent association cortex from BA 37,39, and 40 because lesions that include these areas produce Wernicke's aphasia. -Broca's and Wernicke's are connected through the arcuate fasciculus. Function: -Wernicke's area is mostly in the left hemisphere because language is mostly lateralized to the left hemisphere: Language is subserved by the left hemisphere in 98% of RH males, 90-95% of RH females. 1/3 of LH left hemisphere; 1/3 of LH right hemisphere; 1/3 of LH both hemispheres. Language is different from speech: Speech is is supported by the entire motor system for vocalization.

Cerebral Asymmetry SLIDE 19 /Pic (slide 17 pp) 1. Anatomical and Functional Functional Asymmetry:

1. Anatomical and Functional Left and right sides are not identical. The anatomy of the left vs right the sulci and gyri are not identical, lateral fissure is straight but on left it is curved. Purple Left primary auditory is one strip, on the right it is two Functional Asymmetry: o Left= verbal o Right= non-verbal o SLIDE 20 PIC (slide 18 pp)

Damage of other regions give rise to different forms of visual agnosias: (slide 15 pp)

1. Object agnosia= bilateral inferolateral parts of occipital lobes (Face and object recognition areas). Patient fails to name or indicate the use of a seen object. Vision is intact because patient can see an object but can't tell "what" it is. If the object is touched, or smelled, or make a sound with it (i.e., bringing another sensory modality), then the object is recognized. Blue is problem recognizing faces-prosopragnosia or objects Lose ability to recognize colors from stroke, damage in v4 area: achromatopsia

Key functions in temporal lobe (slide 8 pp) 1. Primary Auditory cortex (Transverse Gyri): Lesions

1. Primary Auditory cortex (Transverse Gyri): o The primary auditory cortices (areas 41 and 42): o Represent the acoustic frequencies and intensities of a large range of pitched and unpitched sounds (speech, music, environ-mental noises) so as to permit their recognition and spatial localization o Each auditory cortex receives information from both ears o Therefore, unilateral damage does not cause deafness (still disrupts hearing though) o Surrounding the primary auditory cortex in the posterior and superior parts of the temporal cortex, there is an association auditory cortex Lesions: In bilateral lesions: auditory agnosia Unilateral lesion in dominant hemisphere (left): pure word deafness This is an agnosia restricted to words. The patient does not recognize speech sounds, but can recognize non speech sounds, and can produce normal speech. If the lesion is slightly more posterior, you get Wernicke's aphasia. (can't comprehend words) Unilateral lesion in the same area in the non-dominant hemisphere: amusia Inability to produce and recognize musical sounds

2- His gaze was consistently directed toward his right and he was unable to bring his gaze past the midline when asked to look to the left. When he was asked to look at the examiner, who then passively rotated his head in the horizontal plane, his eyes moved conjugately and fully (i.e., his gaze paresis could be overcome by the doll's-head or oculocephalic maneuver). His visual field defect is shown in Figure 7-1. pp 22

2- Voluntary move eyes based on a command look with your eyes left/right, requires a command from the cerebral cortex (top of brain). Gazed to the right and eye wouldn't move past midline. When examiner moves the head for the patient, the eyes should rotate to stay on the target, oculocephalic maneuver, done in the brainstem with cranial nerves 3, 4, and 6. To move the eye to gaze it is 6 and 3 for lateral and medial movements. Two different mechanism of gaze and eye movements. Cerebral cortex is probably what is affected here. Slide 2 on 4b - cortical cant move eyes laterally, brain stem dolls head maneuver the eyes will not turn and gaze, they go with the head. Why it's directed to the right: How can localization of lesion to cortex rostral to the right thalamus be consistent with visual deficits? Left gaze palsy: Pathway for control of horizontal gaze begins in frontal eye fields (FEF)- anterior to the motor facial representation of the precentral gyrus. Frontopontine tract (part of the motor system) descends from motor cortex and reaches the PPRF on the contralateral side. Lesion will cause eyes to deviate to the side of the lesion. IN patient, lesion above the lower midbrain of pathways from FEF will prevent patient from being able to make left gaze.

3- His visual field defect is shown in Figure 7-1. pp 23

3- Visual field defects: the circles are the visual field, the black dots are blind spots. To test, ask if you see hand in the 4 corners of the visual field, this is imprecise, the precise way is to put eyes in machine, look at something, flash lights in areas and ask to see if they see the stimulus, over the entire visual field. Left sided hemianopsia Slide 3 on 4b. Somatotopy in visual system as well, nerve fibers from medial side of eyeball stay medially where nerve fibers from lateral side of eyeball stay laterally. When nerves from medial go to chaism, they cross. Lateral nerves do not cross. Optic tract have nerve fibers from lateral side of one eye and medial of the other. Lateral part of retina carries medial side of visual field. This is left sided homonymous hemianopsia Damage anywhere on the right side (parietal cortex stroke) will give the same thing anywehere from optic chaism to visual cortex. If damage visual cortex, there is only center/fovial visual spared, because there is blood supply from two dif areas since it is at the tip

4- The muscles of facial expression in the lower portion of the left face were moderately weak and there was moderate weakness of the left arm and mild weakness of the left leg. pp 24-26

4- Face has muscle weakness on left lower part, central facial palsy. Slide 4 on 4b, Because the fibers are crossed/uncrossed for upper, and lower are only crosses so lesion in the brain only affects the lower part. 4. Motor Function of CN VII: All muscles of facial expression -Corticobulbar fibers go: •to upper face: are crossed and uncrossed. •to lower face: are crossed -Significance? corticobulbar lesions (supranuclear) - contralateral muscle weakness in only lower face (Central facial palsy) -Efferents are to muscles of facial expression: Lesions involving facial nucleus or nerve: Ipsilateral paralysis of facial muscles (Peripheral palsy): both the upper and lower facial muscles are affected. Testing facial muscles on Slide 5 on 4b ADD words, slide 6 difference between peripheral facial nerve palsy and central facial nerve palsy. Some paralysis on left side.

5- On the left side, the tendon reflexes were hyperactive and Babinski's sign was present

5- Upper motor neuron signs: due to lesions involving lateral corticospinal and descending motor tracts -Loss/paralysis or dimunition (paresis) of movement -Increase in muscles tone (spasticity) -Hyperreflexia (exaggerated deep tendon reflexes) -clonus -Abnormal superficial reflexes -Babinski sign: makes toes curl -All are ipsilateral when lesion is in the spinal cord and below the level of the spinal cord region -neuron 1= upper motor neuron: neuron in primary motor cotex descend ipsilaterally and cross at the midline in the medulla, then continue descending the spinal cord and either leave the tract to terminate directly or indirectly on neuron 2 Lower motor neuron signs (due to lesions involving anterior horn cells): -Paralysis or paresis of movement -decrease in muscle tone -Hyporeflexia (decrease in deep tendon reflexes) -Spontaneous activity of muscle fibers at rest -Muscle atrophy -neuron 2= lower motor neuron: anterior horn cells that innervate skeletal muscles

6- Light touch, pinprick, and warm and cold stimuli were accurately identified over the face and limbs. With his eyes closed, however, he was imprecise in localizing where on his left limbs a particular stimulus was applied.

6- Temp and pain was receptive, but spinothalamic tract may be affected, bc conscious prociception is in spinothalamic tract which this is affected, and with a lesion here you lose ability to recognize fine qualities of pain but can feel light pain. Really cannot tell when eyes closed.

7- Proprioceptive sensation was impaired on the left side. With his eyes closed, he was unable to trace coins placed in his left hand (astereognosis) or to name figures traced in the palm of his left hand (agraphesthesia).

7- Proprioceptive sensation was impaired on the left side. With his eyes closed, he was unable to trace coins placed in his left hand (astereognosis) cant feel shapes or to name figures traced in the palm of his left hand (agraphesthesia) cant feel tracings of letters. Dorsal column medial leminiscus system important in this

8- With his eyes closed, he was able to identify which of his hands was individually touched by the examiner. However, when both hands were touched simultaneously, he stated that only the right side was touched (left sided extinction to double simultaneous simulation).

8- If touch both right and left leg at the same time, patient only feels right leg. This is a neglect. Neglect only happens on the left side

Condition Chart (slide 16 pp) Don't need to memorize anatomy area/names..... Achromatopsia, Visual agnosia, Prosopagnosia, Anton's syndrome

Achromatopsia: failure to recognize color. Lesion in inferior occipital cortices, sparing calcarine cortex. 1. lesion causes R hemi-achromatopsia and vice versa Visual agnosia (objects): failure to recognize objects, but able to describe their physical structure. Lesion in bilateral inferior occipital cortex, sparing calcarine Prosopagnosia (faces): failure to recognize faces, but able to see the face. Lesion in bilateral occipitotemporal Anton's syndrome: denial of blindness. Lesion in bilateral occipital cortices from calcarine and extending superiorly to parietal cortex

Acute middle cerebral artery stroke pp55-56 Acute stroke with edema Posterior cerebral artery Lacunar stroke pp57-63

Acute middle cerebral artery stroke SLIDE 18-19: -Tissue looks white. Sometimes the contrast isn't great, so you flip it so tissue would be black slide 20, now can see the damage better. Acute stroke with edema: -Most obvious complication is swelling or edema, SLIDE 21. No place for brain to expand so swelling creates pressure and problems/death Posterior cerebral artery: -Yellow SLIDE 22-23, occipital cortex damaged -Chronic ischemic stroke: Encephalomalacia, SLIDE 24, damage that causes prosopagnosia, bilateral fusiform gyrus, VERY rare to have stroke in same place on both sides bc of different arteries Lacunar stroke: -Small penetrating arteries, SLIDE 26-27 -Common with diabetes

Genes Linked to AD

Amyloid Precursor Protein (APP): familial early onset of AD Presenilin (PS) 1 and 2: familial early onset of AD Down's Trisomy 21: link to early onset of AD ApoE4: increases the risk of late onset of AD Tau (MTAP): mutations on Tau are linked to Fronto Temporal Dementia, but not to AD.

Language Anatomy and exam Peri sylvan language structures PP 44

Anatomy Left hemisphere Exam o Fluency o Naming o Repetition o Comprehension o Reading o Writing Peri-Sylvian Language Structures o Brocca's area (front, can understand but cannot answer back words don't make sense), back is Wernicke's (fluent speech but no comprehension and lack of awareness of this problem), and the arcuate fasciculus. o Left temporal parietal damage o Parietal damage

Visuospatial/perceptual Anatomy and exam

Anatomy Right hemisphere damage Exam -Copy of geometric designs: Ex. Neglect: space and object, with stick figures does not draw left side, only draw right side of pictures -Judgment of line orientation Ex. Put a cross through every line you see here, only does the right side, neglects the left side. Albert's Line Cancellation: Sensitive to Neglect -Object/face/color recognition Graphesthesia: tracing?? Asterognosis: recognize objects from touching them

Attention Anatomy and exam

Anatomy o Focal (cortical or subcortical): Neglect, don't pay attention to one part of their world (usually left) o Diffuse (metabolic, toxic, infectious): Drunk, diseases with those metabolic, toxic, infectious Exam: o Observe patient o Orientation (person, place, time) • Do they know who they are, where you are, and what time is it/date/day of week

Memory Anatomy and exam Memory encoding network PP 45

Anatomy o Medial temporal lobes o Thalamus: Anterior thalamic nucleus (possibly medial) carry memory and limbic functions o Basal forebrain Exam o Remember 3 words 5 minutes o Remember 3 shapes 5 minutes o Past public and personal events (retrograde memory) o Factual knowledge (name last president of the US) Memory encoding network SLIDE 6 o Medial temporal lobes: The hippocampus is in here o Thalamus: Anterior thalamus, and some medial o Basal Forebrain: One source for acetocoline: excitatory neurotransmitter, voluntary muscle movements, memory/attention/learning. Early aspects of alzheimer's begin with degeneration in this system. Current Az drugs tend to be polyergic agonists, trying to boost acetocoline

Executive function Anatomy and exam

Anatomy: Frontal lobes damage Exam -Affect: frontal lobe functioning, mood, lose their ability to express emotion. -Verbal fluency: speaking fluently, brocca's area is in frontal lobes -Sequential motor ability -Delayed alternation -Snout (puckering lips), suck, grasp, rooting (scratch cheek, turn towards that side): these reflexes mature the latest, so when there is damage here you begin to see these frontal lobe signs—frontal release signs are disinhibition of these reflexes

Damage on the left parietal cortex

Aphasia: loss of ability to understand or express speech, Patients with similar damage on the left side of their brain, they are usually cognizant of their deficit and often feel depressed.

Higher order cerebral function

As we shall see higher order cerebral functions (such as reading) depend on both local cortical functions (vision) together with more distributed cortical network functions (language)

Unimodal and heteromodal association cortex

Association cortex can be divided into unimodal (modality specific) association cortex and heteromodal (higher order) association cortex. DON'T MEMORIZE THE ALTERNATIVE NAMES for primary and sensory motor cortex Primary sensory and motor cortex- also known as idiotypic cortex or heterotypic cortex Primary sensory cortex- aka koniocortex, hypergranular cortex, granual cortex. Ex. Primary somatosensory cortex, primary visual cortex, primary auditory cortex Primary motor cortex: aka macropyramidal cortex, agranular cortex. Ex. Primary cortex Association cortex aka homotypic cortex Unimodal association cortex: aka modality-specific association cortex. Ex. Somatosensory, visual, or auditory association cortex, premotor cortex, supplemental motor area Heteromodal association cortex: aka higher order association cortex. Ex. Prefrontal cortex, parietal, and temporal heteromodal association cortex. Multiple modalities that come together

4. Why is the patient's gaze directed to the right?

Bc damaging right frontal eye field. Damaging this area (the frontal eye field) if ask to move eyes to the left side you cannot do it. It deviates to the side of the lesion. Need frontal eye field to voluntarily move to the left side. Can overcome this by the dolls thing. When examiner moves the head for the patient, the eyes should rotate to stay on the target, oculocephalic maneuver, done in the brainstem with cranial nerves 3, 4, and 6. Slide 10. Cerebral is for voluntary gaze.

(slide 14 pp) Damage involving multimodal association cortex

Beyond the primary visual cortices, damage to cortical areas begin to cause visual disturbances that are not associated with blindness—these are usually damage involving multimodal association cortex: Two streams of information: the "what" and "where" pathways. What: you can describe the object but cannot tell what the object is. Prosopragnosia: can't recognize faces, not being able to see. Where: cannot identify the location of objects

Nomenclature SLIDE 2 picture Brodmann's vs named sulci and gyri

Brodmann areas: were originally defined and numbered based on the cytoarchitectural organization of neurons using the Nissl method of cell staining. Many of these areas defined solely on the basis of their neuronal organization have been correlated closely to diverse cortical functions: For example, Brodmann areas 1, 2 and 3 are the primary somatosensory cortex; area 4 is the primary motor cortex; area 17 is the primary visual cortex; areas 41 and 42 correspond closely to primary auditory cortex; and Broca's speech and language area correspond to the left Brodmann areas 44 and 45).

5. Why does the patient have a left gaze palsy?

Can't move eyes to the left, frontal eye field

4. Coordination, Balance, and Gait pp 35, 36, 37 Cerebellum, Coordination and Gait tests

Cerebellum o Feedback control: go to the target o Intention tremor with cerebellar disease: it is not a straight line, you have intention tremor to try to get the target o Cerebellar atrophy (usually developmental problems) vs normal cerebellum SLIDE 46-47. Hemorrhage from stroke: blood looks white when this happens Coordination and Gait tests o finger to nose/heel to shin testing o simple and complex finger movements o three step motor movements: hands on knees, flip them over, lift them up. It would be hard for people with this problem to do o heel to toe walking o Romberg test: lose balance when eyes are closed

Treatment of Alzheimer's disease Degeneration of Basal Forebrain Nuclei Loss of Acetylcholine

Cholinergic replacement Anti-amyloid agents http://www.nature.com/news/alzheimer-s-drugs-take-a-new-tack-1.11343 -Prevent the plaque / beta amyloids are the problem -Unfortunately, the clinical trial of this tx./approach does not seem to work very well as seen in the link. Degeneration of Basal Forebrain Nuclei Loss of Acetylcholine: 6b slide 10 -Memory loss is due to the degeneration of the basal forebrain/ loss of acetylcholine. -Acetylcholine important for memory so if they are degenerating, they want to replace as a therapy.

Clinical Manifestations of Congenital Aneurism Rupture The fix clip SLIDE 39 p72-74

Clinical Manifestations of Congenital Aneurism Rupture: -SLIDE 37, ADD WORDS -First: very severe headache/worst of lifetime. Can lose consciousness. Signs of meningeal irritation get constant flexing of the legs. Spinal tap here to confirm a bleed in subarachnoid space. Red it is still fresh blood and still bleeding, when it is yellow, bleeding is beginning to stop. Clear is when back to normal Acute subarachnoid bleed SLIDE 38, white is all blood

Alzheimer's Cognitive and behavioral deficits

Cognitive deficits -Profound memory loss (anterograde/retrograde) -Language - anomic, empty, circumlocutory (cannot express themselves) -Visuospatial disturbance -Most telling sign - they leave the house but they don't know how to get back and they can be right in front of the house Behavioral deficits -No significant early changes in personality -Unawareness or denial of illness -Psychosis: this is because they get scared and remember things. They get shocked, agitated or angry and may become paranoid. No sensory or motor deficits! (NO paralysis!) Age of onset 70s - 80s: Can happen earlier but rare!

Pick's disease/frontal dementias Pathology of Pick's disease cognitive and behavioral deficits what happens to the brain physically? p79-80

Cognitive deficits -profound executive dysfunction -good memory, language problems (aphasia due to broca's area), visuospatial skills (preserved early on!) Behavioral deficits -early prominent personality changes -poor judgment, insight, disinhibited, labile, euphoric, socially inappropriate, sexual indiscretions Frontal release signs (grasp, snout etc.) on neurological exam but no sensory or motor deficits Age of onset 50s - 60s 6b slide 14: Gyri wide in particular areas ( frontal lobe) Pathology of Pick's disease: pick's bodies slide 15

Coma requires Evaluation

Coma requires: Damage to reticular activating system: all sensory systems ascending to the brain. Brainstem: medulla, pons, midbrain Both hemispheres impaired Still some brain activity, still some reflexes seen in the brain, can evoke potential EEG activity Evaluation: • Cranial nerves: are any abnormal then consider problem in brainstem • Pupil reflexes- midbrain problem • Breathing patterns - all brainstem • Posturing: De corticated- midbrain. De cerebrate- pons

2. At what level of the CNS are they affected? pp 27

Cortex, slide 9, it has to be above the pons so most likely in the cerebral cortex.

2. Medial temporal lobe: (slide 9 pp) when damaged

Cortical and subcortical structures of the limbic system Entorhinal cortex (area 28) Hippocampal formation Amygdala Entorhinal cortex and hippocampal formation - memory. When damaged: Anterograde memory impairment (bc of the hippocampus) Amygdala - attaching emotional significance to events. When damaged, there is a marked decrease in the ability to express emotions. Normally you can recall events with emotion better than events that did not have an emotional attachment Kluver-Bucy syndrome: resulting from bilateral lesions of the medial temporal lobe (including amygdaloid nucleus). Klüver-Bucy syndrome may present with hyperphagia, hypersexuality, hyperorality, visual agnosia, and docility.

Questions you need to know for exam 1. What functional sensory and motor systems are affected in this patient?

Corticospinal tract - left-sided weakness of the leg and arm, hyperreflexia and Babinski sign, and weakness of the lower portion of the face suggest upper motor neuron lesion. Where is the likely site of damage in the corticospinal system? Involvement of both arm and leg indicates Lesion at or above the C4 level in the spinal cord. However, left sided facial Weakness localizes the lesion Above the level of the facial Nucleus in the pons. Thus, the motor lesion Must be rostral to the lower pons . Somatosensory information conveyed through spinothalamic and medial lemniscal systems. Spinothalamic system mediates pain and temperature Sensation, in patient no deficits in these functions Patient could feel these stimulations, but with eyes closed Was unable to accurately locate the source of the stimulus. Patients with lesions to the somatosensory cortex That spare the thalamus can have touch, Pain, and temperature sensations (elementary sensations), but may not be able to precisely localize the area being stimulated. Discriminative sensations (proprioception, steriognosis, Graphesthesia, etc.) require intact medial lemniscal system and was impaired in the patient's left side. Intact elementary sensation, but impaired discriminative Sensation suggests a lesion of right hemisphere rostral to The right thalamus.

5a Neuro Exam In neurological exam look to assess the 5 broad functions

Cranial nerves: almost all are located in brainstem, are they normal Motor system Sensory system Coordination/balance/gait: basal ganglia mostly here Mental Status: cerebral cortex

Criteria for brain dead The Mental Status Exam- Assessment of the Cerebral Cortex

Criteria for brain dead • Def: no neurological activity above the level of the medulla • Pupils fixed and dilated • All facial muscles not responding • No brainstem evoked potential The Mental Status Exam- Assessment of the Cerebral Cortex 1. ATTENTION 2. LANGUAGE 3. MEMORY 4. VISUOSPATIAL 5. EXECUTIVE FUNCTION

5b Neuro exam Coma 5. Mental Status: cerebral cortex and coma By brainstem

Damage in the back/dorsal is coma Damage in the front/ventral is locked in Thalamus is right here, when you have large bilateral thalamus damage you can go into coma Cortex can get lots of strokes Consciousness is almost synonymous with being able to sense body sensations (sensory and visceral) any time you disconnect this sensation you have a loss of consciousness

In the non-dominant (right) hemisphere: involving the inferior parietal lobule: the superior parietal lobule

Damage to areas involving the inferior parietal lobule: Anosagnosia: denial or unaware of illness Left visual field neglect. A compromise in: o The ability to take a route without hitting obstacles placed on the left side of the body. o The skill to follow a previously known and automated route (in a house or a town) o The capacity to learn a new route. o The patient looks confused Damage to the superior parietal lobule: Optic ataxia

PET Glucose in Dementia pp81 Severity and time of neurodegenerative disorders and multi infarct dementia pp82

Difference between pick's and alzheimers slide 16: -NEED glucose everywhere. -Pick's Disease (blue = no activity) dead activity in frontal lobe -Alzheimer's: activity in the frontal lobe, no activity in the temporal lobes Vascular (multi-infarct) dementia slide 17 Severity and time of neurodegenerative disorders and multi infarct dementia: slide 18, neuro is steady linear decline over time, multi is fine, stark decline, stay at same level for a bit, stark decline, stay at same level for a bit, etc -Steady decline in the neurodegenerative: neurons die slowly and constant -Multi-infarct Dementia: they come and go in burst. So when measuring cognitive decline it is seen as a step decline.

CN VI Abducens nerve lesion

Enervates the lateral rectus With lesion here Medial strabismus: The medial rectus muscle is unopposed and pulling the eyeball medially.

Extradural (epidural) hemorrhage Subdural hemorrhage PP47

Extradural (epidural) hemorrhage: -Damage to branches of the middle meningeal artery (and vein) can occur following even minor head trauma. -Bleeding tends to extend into the extradural space forming a potentially fatal extradural hematoma (an example of a space-occupying lesion - see below). -Because of the tight attachment of the dura to the skull, these hematomas tend to form slowly and clinical signs may not appear for hours, even days, after injury. Subdural hemorrhage: -The arteries and veins of the brain are located beneath the arachnoid in the subarachnoid space. -However, some superficial cerebral veins pierce the arachnoid and bridge the subdural space to enter the superior sagittal and transverse sinuses. -Subdural hematomas can form in the subdural space if the bridging veins are torn in head trauma. SLIDE 6 PICTURE

CN VII Facial Nerve 2 types of palsy

Facial nerve Bell's Palsy: peripheral, both upper and lower on one side of face is paralyzed. Lower motor neuron forehead paralyzed as well as bottom Central nerve palsy: lower facial muscles paralyzed, not upper, on one side. Lesion is on the right side in the brain. Upper motor neuron forehead spared

Atherosclerosis: thrombus and embolism pp51-52

Fat deposits start to build up in the arteries SLIDE 14 As long as the fat is smooth it does not block blood flow, when cholesterol circulates, it triggers an injury to the pockets of fat and creates divots in these fat deposits. Then platelets come in and lead to blood clot build up Blood clot can get so big and block the artery completely (thrombus) OR A blood clot breaks away (embolus) and clogs up some other artery SLIDE 15 another view of this process

Corticospinal tract (motor system) Grading muscle strength

Goes from motor cortex, goes down ventrally, then to pyramids, then a majority cross to the other side. Upper motor neuron legion is if its damaged in spinal cord, damage in nerve or dorsal horn it is lower motor neuron legion. Grading muscle strength: 0 no movement 1 muscle twitch, no movement of limb 2 muscle contracts but no movement against gravity 3 able to provide minimal resistance 4 able provide moderate resistance 5 normal strength Muscle Tone Normal Decrease - flaccid (lower motor neuron) Increased - rigid, spastic, cogwheeling (upper motor neuron)

Hemorrhagic Stroke (17%) Four types of hemorrhagic stroke

Hemorrhagic Stroke (17%) -Bleeding into the brain substance or around the brain. Four types of hemorrhagic stroke -Intracerebral Hemorrhage -Subarachnoid Hemorrhage -Extradural (epidural) hemorrhage -Subdural hemorrhage

Language areas are not only in the frontal lobes Anatomy Function

However Language areas are not only in the frontal lobes. In addition, we have: SLIDE 13 pictures (slide 12 pp) Wernicke's and sensory language area. Anatomy: -Wernicke's area corresponds to BA 22 (posterior 2/3 of superior temporal gyrus). -Many authors also include in Wernicke's area a rim of adjacent association cortex from BA 37,39, and 40 because lesions that include these areas produce Wernicke's aphasia. -Broca's and Wernicke's are connected through the arcuate fasciculus. Function: - Wernicke's area is mostly in the left hemisphere because language is mostly lateralized to the left hemisphere: - Language is subserved by the left hemisphere in 98% of RH males, 90-95% of RH females. - 1/3 of LH left hemisphere; 1/3 of LH right hemisphere; 1/3 of LH both hemispheres. People with language in both hemispheres, are lucky bc if they damage one hemisphere they are likely to have spared functions from the other hemisphere - Language is different from speech: Speech is supported by the entire motor system for vocalization.

Types of Stroke Ischemic (83%)

ISCHEMIC (83%) or Hemorrhagic Stroke (17%) Obstruction of a blood vessel supplying the brain by a blood clot deprives the brain of essential nutrients and if blood flow is not restored quickly leads to irreversible damage to the area of the brain supplied by the blood vessel. The clot may develop in the blood vessel itself (thrombus) or may arise elsewhere and lodge in the blood vessels of the brain (embolus).

CN IX, X, XI, XII

IX glossopharyngeal nerve and X vagus nerve, deal with the pharynx: mostly sensory and motor. Test for them: look for asymmetry of uvula in pharynx are hanging symmetrically or hanging to one side. Gage reflex XI accessory: evaluate the spinal portion, sternocleidomastoid and trapezius XII hypoglossal nerve: tongue. If there is a lesion, the tongue will deviate towards the side of the lesion. Atrophy, fibrillations

Blood vessels have specific anatomic distributions Posterior cerebral artery Anterior cerebral artery Middle cerebral artery Risk factors Left sided anomilous hymianopsia

If signs and symptoms due to lesion of artery, then localization of lesion must be consistent with the territory supplied by an artery. PCA supplies visual cortex, upper brainstem, and inferior temporal lobe. Does not supply sensory or motor cortices. ACA supplies frontal and medial cerebrum. Strokes there produce lower extremity sensory and motor loss. MCA supplies lateral aspects of cerebrum, including most of sensory-motor cortices and FEF. As well, it supplies the underlying white matter, such as the optic radiations. Thus, stroke In this area could produce the pattern of signs and symptoms observed in the Patient. Middle cerebral artery (lateral surface of the brain) In this example, acute stage causes inflammation so weakness of leg as well. Hypertension and diabetes Are risk factors of atherosclerotic Disease, but patient also had Arterial fibrillations, thus the cause Of the stroke was determined to be An embolus from the left atrium to the Right MCA. Left sided anomilous hymianopsia: bc you Hit the optic tract before it gets to the visual Cortex. Travel through the middle cerebral Artery or lateral part of brain and hit those pathways

Growth of dementia population 6B slide 1 Alzheimer's Age groups

In 1900s 5 million, 2000 40 million, by 2050 80 million. The percentage is rising across generations so in 1900 2% had it, 2000 12%, 2050 23%. Some statistics that show people are living longer (exponential growth in number of people living over 65 years old) Alzheimer's is increasing at this similar rate too. People living older shows that there is a rise in dementia. The incidence goes higher is definitely in the individuals 85 years or older (seen in red) Alzheimer's disease: hit older people, but does not mean it cannot hit people younger than 65. - People who are younger and diagnosed is rare and can be due to genetics. Increases with age, a lot at 60-65, but by 85+ its enormous

Stenosis or occlusion of carotid artery SLIDE 16-17 p53-54

Internal carotid artery, blood flowing through the neck Stenosis with Bruit (hearing abnormal sounds with the stethoscope) Reduced blood flow to that area Circle of Willis can usually compensate for this but you do not want to leave this as a risk. Do a carotid endarterectomy -Go into internal carotid artery and remove the extra fat and leave a stunt

Reversible causes of dementia

Intoxications -Delirium Metabolic Abnormalities: -Renal Failure -Substrate deficiencies (B12/folate deficiency) -Hypothyroidism Depression (pseudodementia) Infectious agents: -Neurosyphilis/fungal meningitis/HIV. Nonspecific toxic agents but become toxic to the neurons which is why if you control them then you can reverse the dementia.

Intracerebral Hemorrhage cause, what is it, differentiation, other common causes

Intracerebral Hemorrhage -Hemorrhage from blood vessels inside the brain -The most common cause of Intracerebral hemorrhage (or bleeding into the parenchyma of the brain) is hypertension (60%). -Small penetrating arteries (in the putamen, thalamus, pons cerebellum) are affected and rupture with bleeding. Patients may have headache, nausea or vomiting and a focal neurologic deficit. -It may be clinically difficult to differentiate between a hemorrhage and an ischemic stroke (about 70% accuracy) so a CT scan of the brain is done urgently to look for bleeding in all patients with acute stroke. -Other common causes of Intracerebral hemorrhage include rupture of an arteriovenous malformations (where artery/veins meet are malformed, they are leaking) , bleeding into a brain tumor, coagulation defects (due to medications such as warfarin, thrombolytic drugs, or in patients with hematologic disorders), or vasculitis.

Mechanisms of stroke Ischemic Hemorrhagic pp48

Ischemic -Thrombotic (60%) an artery with a thrombus growing in the artery until it blocks the artery completely. The black area depicts part of the brain that will die. SLIDE 8 -Embolic (20%) clot carried from the heart, the embolus, gets dislodged from wherever and travels the arteries until it gets into a very small artery and gets stuck, preventing blood from flowing, black part makes brain die. SLIDE 8 Hemorrhagic (20%) -Subarachnoid hemorraghic stroke, blood all in brain SLIDE 8 -Intra cerebral, local artery bursting in basal ganglia SLIDE 8 -These do not kill the tissue, and have a high likelihood of surviving

Four major types of ischemic stroke • Atherothrombotic • Cardioembolic

Ischemic types: • Atherothrombotic • Cardioembolic • Small vessel disease or lacunar stroke • Other causes Atherothrombotic - Atherosclerosis affects the major extracranial (origin of the internal carotid, origin of the vertebral arteries), intracranial arteries (basilar, carotid siphon, origin of the middle and posterior cerebral arteries), as well as the aorta prior to the takeoff of the major vessels. Atherosclerotic plaque ruptures causing platelet aggregation and thrombus formation can develop directly on the plaque in the intracranial vessels. This is the most common type of stroke in those over the age of 50 years. Major risk factors include hypertension, smoking, diabetes and elevated cholesterol. Risk for recurrent stroke is reduced using antiplatelet therapy (e.g. aspirin). Cardioembolic - A thrombus (clot) can arise in the left atrium (atrial fibrillation), left ventricle (after a myocardial infarction or with a cardiomyopathy) on the mitral or aortic valve (endocarditis, rheumatic heart disease), or less commonly in the venous system or right heart with a right-to left shunt (paradoxical embolus) and then tends to lodge at branch points in the cerebral blood vessels. Multiple strokes in different arterial territories suggest this subtype. This is the second most common type of ischemic stroke and is treated with anticoagulation therapy (warfarin) to prevent recurrent stroke. Venous clots tend to end in lungs, embolus.

3. Discuss the patient's visual sensory deficit and provide the appropriate neurological/opthamological name for it. pp 29

Left sided homonymous hemianopsia. SLIDE 12, how neurons from retina are organized as they go to visual cortex, neurons from lateral retina stay on the same side, but neurons from medial retina cross over to the other side. Right side of brain- have neurons from lateral part of right eye and medial part of left eye

Association sensory cortex (slide 13 pp) superior and inferior parietal lobules Lesion Left hemisphere

Lesion: In the dominant (left) hemisphere: (dominant means the language hemisphere, which is usually the left) Damage to inferior parietal lobule: likely to damage connection between wernickes and broccas which will get conduction aphasia (understands what youre saying, can speak fine, but cannot repeat words after you) Angular gyrus- alexia and agraphia. Can have lesion in this area that the person has alexia: can't read written material. If interrupt communication between occipital lobe to wernickes area cannot translate the visual into language Supramarginal gyrus-conduction aphasia Alexia or Dyslexia= Inability to read written language Two types: • Acquired: get a stroke and cannot read, alexia • Developmental: born and grown up with problems in that area, dyslexia • Agraphia= Inability to write language, need motor cortex and this connection is disrupted with broccas area Damage to superior parietal lobule: Optic ataxia in contralateral hand. Optic ataxia: using visual system and motor system, cannot smoothly go and grab computer, its like being in a dark room trying to look for something, rely on sensory system to do it

Lesion immediate stage later stage

Lesion: varied degrees of focal impairment in sensation on the contralateral side of the body: In the immediate stage (acute): Loss of all sensory modalities on contralateral side of body and/or face. In the later stage (chronic): Recovery of sensation of paid and temperature and crude touch sensation. This is because: • Sensation of pain and temperature - thalamic level (when lesion have hard time locating the pain) • Source, quality, and intensity of pain - sensory cortex. • Insula and SII: Asymbolia for pain—Lack of Motivation to avoid pain - • But also anterior cingulate - frontal lobe-has been implicated.

With issues in motor system, what should you look for?

Look for limb movement and especially fingers and thumb: decorticate thumb, stays sticking in Look for tendon reflexes Look for abnormal reflexes. No reflex its lower motor neuron, exaggerated is upper motor neuron Babinski sign: toe sticks up/out, normal reflex is for toes to scrunch in/down

Lesions cont... Continued loss of fine aspects of tactile information on contralateral body (arm and face) so this is the dorsal column medial leminiscus system:

Loss of two-point discrimination Agraphesthesia (inability to recognize a letter outlined on the skin Astereognosis (inability to recognize form, can't identify an object) Loss of vibration and light touch Continued loss of proprioception in contraletral body (arm and face). If leg is involved, you see positive Romberg sign (ataxia when eyes are closed, when take away visual system you lose balance)

2. Motor system evaluation pp 33

M1 is the primary motor cortex SLIDE 9 red part Has a homunculus: foot/leg on medial side of brain, hands on lateral sides, and face below that. Highly developed and sensitive functions in hands and mouth so they are bigger represented in the homunculus

Mechanisms of Hemorrhagic stroke Causes of hemorrhagic stroke p64-71

Mechanisms of Hemorrhagic stroke Hemorrhagic: -intracerebral: blood will burst in brain -extracerebral: • subarachnoid hemorrhage • subdural hematoma • epidural hematoma SLIDE 28- intra cerebral hemorrhage also 29, 30 Causes of hemorrhagic stroke: -Arteriovenous malformation: arteries and veins should blend smoothly, but here create globules of vessels running into each other abnormally and causing leaks. Thin walls. Blood does not flow normally or well. When they bleed it causes the hemorrhage SLIDE 30 -Aneurisms: like to be present where there are branching of arteries. Tend to happen in the circle of willis in the corner of two arteries, could be anywhere but most commonly at the branching of arteries. SLIDE 32-33. -Berry aneurysm on the anterior communicating artery of brain: it is weak and becomes like a balloon. When blood tries to flow through this is gets caught in balloon and hinders blood from flowing and will eventually burst. -Fusiform can happen all along the artery, whole wall abnormal, less normal. SLIDE 34. SLIDE 35 another picture of angiogram- inject die and then take an xray

Causes of dementia

Neurodegenerative disorders (neurons start to die) -Alzheimer's disease: mostly a disease that starts in the temporal lobe. The first sign is memory loss. The famous neural substrates is hippocampus. -Pick's disease: mostly a disease that starts in the frontal lobe. The first sign is personality changes, apathy, dis-inhibition behaviors (doing inappropriate things/ impulsive). Start having language problems due to Broca's area. They may talk and not be able to get to the point. Vascular (multi-infarct) dementia: tiny strokes; tiny holes in the brain Reversible causes: -You can treat the underlying cause; - Can treat the depression to have it go away

Pathology of Alzheimer's 6b slide 6 pp76

Neurofibrillary tangles(tau protein) Amyloid plaques: (beta amyloid)

CN 3 Oculomotor nerve lesions

Ocular muscles: (medial, lateral, superior & inferior rectus, superior & inferior oblique) Every movement besides superior oblique and lateral rectus Lesions of the nucleus or nerve results in Oculomotor nerve (CN III) Palsy: o Ipsilateral lateral (external) strabismus (squint) - eye is down and out o Ipsilateral ptosis - if eyelid is retracted → diplopia o Ipsilateral mydriasis (dilated pupil) o Loss of direct and consensual pupillary light reflexes in the ipsilateral eye

SUMMARY OF BASAL GANGLIA DISEASES Parkinsons, Huntingtons, Cerebellum

Parkinsons: Cause: • Substantia nigra and dopamine (less than 35%) • Basal ganglia (Putamin and globus pallidus) • Hypokinetic disorder Signs o Bradykinesia o Retropulsion: someone pulled you from behind, normal could catch balance by stepping backwards. Parkinsons patients will lose balance/fall o Masked faces: no o Stopped posture: hunching over o Resting tremor: tremor all the time o Led pipe rigidity: spastic paralysis Huntingtons disease: Cause: • Genetic: autosomal dominant, short arm chromosome 4 • Peak onset: 45 years old, highest suicide rate. It happens bc caudate is heavily connected to cerebral cortex • Basal ganglia (caudate nucleus) • Over dopamine, hyperkinetic disorder Symptoms: • Quick jerks, rapid movements • Tone= loose • Towards the end patient has trouble swallowing due to twitching Cerebellum: Symptoms: • Broad based gate • Cant tandem (walk heel to toe on a line) • Speech slurred • Rapid alternating movements off • Intention tremor • Limb control off *alcoholism is a classic disease which cause the atrophy of the vermis

Pathophysiology of ischemic stroke Cellular mechanisms of injury

Pathophysiology of ischemic stroke: -After occlusion of the blood vessel, a central core of tissue has extremely low blood flow (<20ml/100gm/min) and is irreversibly damaged but around it is an ischemic "penumbra" where metabolic activity is reduced but the tissue is still viable if perfusion is restored. Over the first few hours, if blood flow is not re-established, this penumbra shrinks and the central core enlarges. This underlies the principle of treating acute ischemic stroke as an emergency and educating patients to call 911 with stroke symptoms (brain attack). Treatment with thrombolytic agents (tissue plasminogen activator or TPA) to dissolve the thrombus must be within three hours after onset otherwise there is no benefit. -Penumbra is tissue Cellular mechanisms of injury: -After loss of the blood supply there is decreased energy production with failure of ionic pumps and mitochondrial injury. This leads to production of free radicals and activation of leukocytes. There is release of excitatory neurotransmitters (glutamate) which cause further injury with influx of sodium, calcium and chloride ions. This leads to release of proteases which break down the cytoskeleton and DNA. Multiple clinical trials have been conducted looking for drugs which may block these secondary effects (i.e. block the glutamate receptor, inhibit the inflammatory response or block the production of free radicals) but to date no effective "neuroprotective agent" has been found which works in humans (many work in animal models). This is an active area of stroke research. -proteases are what eat the tissues and cause the ultimate problem

Examples of Primary motor and sensory, or unimodal association cortex: (slide 4 in pp) Primary motor area

Primary motor area (area 4 or M1.)= Precentral gyrus It has: o Somototopic maps of contralateral body movements. (homunculus- or body map of primary motor cortex on the brain) o Principal target for cerebellar and motor thalamus projections. Function: It works in association with other motor areas including premotor cortex, the supplementary motor area, sensory and posterior parietal cortex, and several subcortical brain regions, to plan and execute movements. Lesion: varied degrees of focal paralysis in the contralateral side of the body or face. Upper motor neuron lesion

Functionally: slide 6 pic (slide 5 pp) Primary sensory cortex areas 3, 1, 2):

Primary sensory cortex areas 3, 1, 2): Somatotopic maps of contralateral body sensations Received projections from contra-lateral half of the body. This area is interlocked with primary motor cortex, and sends projections to the superior and inferior parietal lobules.

Alzheimer's is Multifactorial !

Reduces neuronal number, snaps number, neurotransmitters: causal genes (21, 14, 1), risk genes (Apo E), head trauma, cerebrovascular disease Increases neuronal number, snaps number, neurotransmitters: estrogen replacement, education, NSAID's Those plus time leads to dementia Left Factors(Causal Genes, Risk Genes, Head Trauma, Cerebrovascular Disease) drive towards dementia Right Factors (DEBATABLE: education [exercise of the brain to resist dementia], NSAID's[non-steroidal anti-inflammatory drugs], Estrogen replacement) drive away from dementia!

6. How would you test this patient's vestibulo-ocular movements? pp 28

Reflex, circuitry between vision and vestibular system. The fluid in semicircular canals send messages to neurons that control eye movement in the brainstem and move eyes accordingly. Dolls head maneuver is a simple test of this. When move head you move vestibular system and causes eyes to move in the opposite direction. Slide 11

7. Why is the abrupt onset of symptoms significant for this patient?

SLIDE 13, when symptoms suddenly appear, this is usually an indication of a stroke-vascular accidents. Seizures. Head trauma. Someone being shot. In this particular case, the symptoms appear suddenly and bc of history of hypertension, diabetes, irregular pulse, most likely a stroke. Abrupt onset on symptoms suggest either vascular or electrical cause (tumors do not *typically* cause abrupt onsets). But signs associated with seizure were not present (e.g. hallucinations and tonic-clonic movements). So cause most likely vascular. But- hemorrhagic or ischemic? -Hemorrhagic stroke commonly linked to increased intracranial pressure and meningeal irritation, not present in this case. -More likely cause of stroke is due to occlusion of arteries. -Hemorrhagic bursts open need a blood clotter, ischemic artery is blocked so blood can't flow through, need anticoagulant therapy. CT scan best to tell which one

3. Sensory System, primary sensory cortex, S1 pp34

SLIDE 38, travels in the back of brainstem, dorsal You check for: o Pain and temperature (spinothalamic)—pin prick o Dorsal medial leminscus column • Vibration/discrimination touch • Proprioception: Romberg sign- lose balance when you close eyes

CN V Trigeminal nerve tests

Sensation on the face, muscles of mastication Tests -Sensory functions: pin pricks, vibration, light touch on various areas of the face. -Moving jaws and asking for direction of movement. -Motor functions: biting, looking for position of jaw (is it deviated to one side?):

What arteries supply what parts of brain Slide 9-10 pp49-50

Slide 9 • Lateral side of brain: middle cerebral artery • Medial side: anterior cerebral artery • Back of brain: posterior cerebral artery Slide 10 • Circle of willis • Vertebral arteries • Middle is to left • Anterior is going up • Posterior cerebral to the right supplying back of brain • These are all penetrating arteries supplying areas to the brain,

Small vessel disease or lacunar stroke Other causes

Small vessel disease or lacunar stroke - hardening tiny blood vessels. lacunar stroke. The blood vessels affected by this subtype of ischemic stroke are the small (100-150µm) blood vessels which are the penetrating branches of the middle cerebral artery (lenticulostriate), anterior choroidal, posterior cerebral and posterior communicating arteries and basilar artery. They are affected by diabetes and hypertension which causes thickening of the vessel wall (lipohyalinosis) leading to occlusion. The infarcts are usually small (15-20 mm) "holes" or lacunes in the putamen, thalamus, internal capsule or basis pontis. They cause approximately 15% of ischemic strokes. With recurrent events, a multi-infarct dementia can occur. Other causes - Stroke may be caused by a number of other causes (more commonly in young patients) including blood disorders such as hypercoagulable state or hemoglobinopathy, dissection of the blood vessel wall due to illicit drugs or an autoimmune process (vasculitis), or obstruction of the veins (venous sinus thrombosis). SLIDE 3 PICTURE, hematologic disease

Commissurotomy (or split brain): SLIDE 21 PIC/words (slide 19 pp) Clinical test

Split brain: cuts the corpus callotum which connects the left and riht hemisphere. Classic problem with this patient is holding something in left hand, name what you are holding in left hand, need sensory it will end up in right side brain, in order to say it need to cross to left side for language, BUT this cross is not available bc of corpus callotum. If in right hand they can tell you what it is bc its already on the left hemisphere Language= left hemisphere -Put object in left hand--sensory information gets to right hemisphere. -Ask patient with split brain to name that object: Cannot name it. -Put the same object in right hand: the patient can name it. Clinical test -The Wada Test: To see on which side is language before surgery -SLIDE 22 pic/words (slide 20 pp)

Slides 6a Stroke A. Stroke B. Transient Ischemic Attack (TIA)

Stroke • An injury to the brain caused by the interruption of blood flow to a focal area of the brain or by bleeding into or around the brain. This causes the sudden onset of a focal neurologic deficit or headache which lasts for at least 24 hours or leads to death. Transient Ischemic Attack (TIA) • Sudden onset of a focal neurologic deficit of presumed vascular origin which last less than 24 hours (most last about 15-20 minutes). Recently, it has been proposed that the definition be shortened to one hour. About ten percent of strokes are preceded by a TIA and the highest risk of stroke is the first week after the onset of TIAs.

Cortical Topography of Alzheimer Pathology Tangles and plaques 6b slide 7 MRI and Hippocampal Atrophy in Alzheimer's 6b slide 8 pp77-78

Tangles - Primary cortices are spared which is why they are not going blind or having sensory/motor deficits. Plaques - medial temporal lobe spared. They have less sparing of the cortices. Alzheimer's mostly start in the temporal lobe and spreads to the rest of the brain. MRI and Hippocampal Atrophy in Alzheimer's 6b slide 8: Using imagining to confirm alzheimer's

Examples of heteromodal (multimodal) association cortex: (slide 11 pp) Prefrontal cortex Anatomy of Broca's:

The areas of the frontal lobe located anterior (i.e., in front of) the motor functional areas (i.e., 4,6, and 8) are considered the Prefrontal Cortex. The prefrontal cortex includes areas that mediate higher mental functions such as: Language areas: Broca's area (Areas 44 and 45) Anatomy of Broca's: • Red and green areas • Lateral (Sylvian) fissure: anterior horizontal, ascending, and posterior limbs. (don't need to memorize this name specifically). This creates: o Pars orbitalis, triangularis, and opercularis o Broca's= triangularis + opercularis • Follow the sylvian fissure and two things that go up and make a triangle (red) which is the triangularis, usually the combination of the red triangularis and green pars orbitalis

Left versus Right hemisphere Lesions: Damage to the right parietal cortex= Anosognosia

The classical clinical condition of patients with parietal damage (involving insula, somatosensory, and adjacent cortices) on the right side is that of anosognosia. Anosognosia means denial of illness or failure to recognize an illness. The condition is characterized by apathy and placidity. The most frequent causes of this condition include stroke, glial tumors, and head injury. The classical example of this condition is that the patient is paralyzed in the left side of the body, unable to move hand, arm, and leg, and unable to stand or walk. When asked how they feel, patients with anosognosia report that they feel fine, and they seem oblivious to the entire problem. Alien hand: think their paralyzed hand is someone else In stroke patients, the unawareness is typically most profound during the first few days after onset. In a few days or a week, patients will begin to acknowledge that they have suffered a stroke and that they are "weak" or "numb", but they minimize the implications of the impairment. They might say: I am right handed, I don't care if my left hand moves or not. In the chronic epoch (3 months or more after onset), the patients may provide a more accurate account of their physical disabilities. However, defects in the appreciation of acquired cognitive limitations may persist for months or years.

SUMMARY OF STROKE Major blood vessels, risk factors, types, warning signs

Three major blood vessels o Middle cerebral artery MCA o Anterior cerebral artery ACA o Posterior cerebral artery PCA The MCA and the ACA both come off of the carotid artery The PCA comes off of the Basilar artery Risk factors for stroke • Hypertension • Increased cholesterol • Smoking • Diabetes • Genetics • Heart disease (embolic) • Hypercoagulable - Sickle cell in kids Types of stroke: • Occlusive stroke (AKA ischemic stroke or cerebral infraction) • Hemorrhagic stroke (AKA reputured aneurism Warning signs • Transient ischemic attack: often before blood vessel closes off, warning signs are given off. Ex. Grandpa may have trouble speaking and right hadn doesn't work. Lasts 20-30 min and then grandpa is ok. • Anuerysm: may get a warning leak. Severe headache out of the blue. Worst of life. - sex, exercise, stimulants

Cranial nerve 2 optic nerve Test for visual activity, look for health of eye, visual field defects pp 32

Try to evaluate vision, visual activity Snellen chart: letters or numbers going from bigger to smaller 20/20, 25/20, 20/40: The numbers you are supposed to be at a distance of 20 feet, if you're vision is 20/20 you can see the smallest line from 20 feet away. 20/40 at a distance of 20 feet, you see what a person would see at 40 feet. At a distance of 25 feet you see what normal people can see at 20 feet Look for health of the eye: eye covered with blood vessels Slide 12 disorders: red lines are blood vessels, white part is the optic disk where all the nerves from optic nerve exit PAPILLEDEMA: optic nerve swelling and DIABETES: hardened blood vessels which can lose your vision Testing Visual Fields and Defects: 1. Confrontation method - done with fingers. It is less precise. 2. Perimetry - done with a computer. It is more precise.

CN IV Trochlear nerve lesion

Turns eye medially and pull it down a little bit In CN IV (or Superior Oblique) Palsy, the patient: o May look like this: turned up and out • When walking downstairs, complaining of double vision (diplopia). Complain of diplopia especially when walking downstairs or reading (requiring eye intorsion). o Tilt head away from the side of lesion (to compensate for the alignment of both eyes and help relief the diplopia) so tilt towards the healthy eye

Midline structures Basal ganglia

Usually these gait and balance disorders are associated with the midline structures of the cerebellum: o VERMIS: Legs and Midline Basal ganglia o Subthalamic nucleus, globus pallidus, caudate, substantia nigra picture of structures in the brain SLIDE 51 and 52, globus pallidus on inside of putamen, substantia nigra down behind it. Substantia nigra connected to caudate/putamen is dopamine- NIGROSTRIATAL PATHWAY. PP 38-39 o Parkinson's is degeneration of substantia nigra SLIDE 50, 55, Progressive changes in posture, gait, and balance in Parkinson's, intention tremor, very little facial expression (masked faces). Early signs: resting tremor, difficulty buttoning shirt, since hand shaking they tend to write in small letters. PP 40-41 o Huntington's chorea: degenerated caudate, degenerates. Normal vs abnormal SLIDE 58-59. PP 42-43

Cranial Nerve VIII Auditory Nerve

Vestibulocochlear nerve Balance and hearing. Mostly look for hearing with this nerve to see if hearing is intact. Deafness is not complete, you can get disorders with hearing but complete deafness usually related to peripheral problems

c. Effects of lesions in Occipital lobe-calcarine: Primary Visual Cortex (slide 10 pp)

Visual cortex is organized by lower visual field by upper parts of the brain and vice versa If lesion in upper calcarine = lower field defect If lesion in lower calcarine = upper field defect Note how the macular (central) vision is mapped towards the tip of the occipital cortex. Therefore, strokes that cause lesions in this area (e.g., PCA strokes) produce visual defects similar to optic radiation lesions, but with one exception: There is macular (central) vision sparing (cortical lesions) Cortex lesions tend to spare central vision because it is represented in an area that receive multiple sources of blood supply (i.e. tip of visual cortex receive blood from PCA and MCA). Macular is being able to see the center of the visual field, mapped in the tip/back of the visual cortex. Posterior cerebral artery (medial) covers the back visual area, outside/lateral of brain the middle cerebral artery covers it, only the tip area can receive blood from middle cerebral artery so seeing center vision is still intact.

Clinical Case 1 Case history

While eating breakfast, a 59 year-old right-handed man with hypertension and diabetes mellitus dropped a glass of juice that he had been holding in his left hand. His speech became slurred, and he noted numbness over the left half of his body. He was able to walk, but he dragged his left foot. His wife, noting no change in his condition over several hours, brought him to the hospital. Notes: Finding the signs of a stroke: FAST, paralysis of arm- A, speech that is slurred. Looks like he might be having a stroke

Somatosensory cortex (slide 7 pp)

Wilder Penfield stimulated the sensory cortex in awake epilepsy patients and had report the sensations they felt: 1. This created a topographical map that represented the body surface on the primary sensory cortex: the homunculus. 2. Penfield also discovered that different body parts had disproportionate cortical representation (e.g., hands are very large). 3. The original "Homunculus" of Penfield remains valid, but subsequent electrophysiological research revealed that there could be as many as 4 humunculi lined up next to each other representing sensations from muscle movement (3a), pain and temperature receptors (3b), discriminative touch (area1), and proprioception (area2).

SLIDE 4- examples of unimodal association cortex and heteromodal association cortex

examples of unimodal association cortex include somatosensory association cortex, visual association cortex and motor association cortex (premotor cortex and supplementary motor area) Red parts are primary cortex Unimodal sensory association receives its predominant input from primary sensory cortex of a specific sensory modality and performs higher order sensory processing for that modality. Unimodal motor association cortex latino the motor program for complex actions involving multiple joints. In contrast, heteromodal association cortex has bidirectional connections with both motor and sensory association of cortex of all modalities. In addition, heteromodal association cortex has bidirectional connections with limbic cortex. This anatomical arrangement enables heteromodal association cortex to quire integration of abstract sensory and motor information from unimodal association cortex, association cortex, together with emotional and motivational influences provided by the limbic cortex. Heteromodal association cortex is found in the frontal lobes and at the pirate-occipitotemporal junctions Primary auditory cortex is the part that is going inside (in the picture) Slide 3 in neuro powerpoint

Cranial nerve 1 olfactory nerve Where, problem, test pp 31

slide 4 the ones coming from the nose are very tiny hair cells that transmits signals to the brain. You go through the pin holes in the skull slide 4, nose holes in the skull. The hair cells from the nose go through this to get to the brain. PROBLEM: if you break your nose, you could cut those little hair cells and the consequence is Traumatic Anosmia Test: A special kit that has numerous packets that store various smells. The examiner scratches one packet at a time and asks the patient to identify the smell. This is done by closing one nostril, and testing the other.

Organization of Somatosensory system

• A. Somatosensory pathways • B. Somatosensory cortex SLIDE 8 Picture (slide 7 pp) c. Effects of lesions in Occipital lobe-calcarine: Primary Visual Cortex SLIDE 11 pic (slide 10 pp)

Risk Factors of Stroke

• Hypertension • Cigarette smoking • Diabetes • Hypercholesterolemia • Overweight/No Exercise