1. Given the clinical presentation of any patient with acute visual loss, be able to recognize the following diagnoses:
a. Migraine-induced visual loss
Disturbance in vision in both eyes
Develop into scotomata
Edges of flashing or zigzag lines
Tunnel vision common
Sympt last 15-20mins and followed by headache, photophobia, nausea.
Vision is recovered.
b. Retinal detachment
Heralded by flashing lights and floaters (black spots that drift about)
Then there is a curtain or shade of darkness over vision in one eye
Visual loss begins in periphery and moves centrally.
If severeàafferent papillary defect develops in involved eye.
SURGERY TO RETACH retina.
c. Amaurosis fugax
painless
transient
monocular vison loss
pts over 50.
“Curtain coming down over vision” which may affect whole visual field, or only the superior or inferior ones.
Attack completes 30secs and may resolve within 10 mins
Increase risk of stroke.
d. Optic neuritis
infl of optic nerve due to MS, infection, vasculitis.
Young patients 20-45
Sudden loss of vision, unilateral
Pain on eye movement
Vision loss becomes maximal over 3-7 days and then stabilizes
May see afferent papillary defect
Can be retrobulbar
Lesion is further posterior to the nerve head.
Vision improves 6-8 wks
Optic nerve becomes ple wks to months after attackàoptic atrophy
MRI if MS for Rx.
e. Arteritic and non-arteritic ischemic optic neuropathy
Non-arteritic: 50 to 70 years.
painless sudden loss of vision in one eye.
entire VF or just the upper or lower half of the VF (hemi- altitudinal defect).
Vision loss is variable and may be minimal (20/30 to 20/40) or severe (counting fingers).
Visual loss remains stable with no recovery.
Initially, the optic disc is pale and swollen with occasional small flame hemorrhages
Optic disc swelling resolves in 4-8 weeks, and optic atrophy becomes evident.
Arteritic:
70 to 90 years of age.
Visual loss is often severe, even to no light perception.
Fever, weight loss, general malaise, myalgias, temporal headache, jaw claudication, and tenderness over the temporal arteries.
High erythrocyte sedimentation rate (ESR)
Generally over 60 mm/hr and usually 90 to 110 mm/hr.
This is a true emergency requiring prompt diagnosis and treatment.
f. Papilledema
swelling of the optic discs due to increased intracranial pressure.
bilateral and usually asymmetric.
must be considered urgent, and the patient should be assumed to have an intracranial mass lesion until proven otherwise. Neuroimaging is mandatory.
If CT or MRI is negative, then further work up including lumbar puncture is necessary to rule out idiopathic intracranial hypertension (pseudotumor cerebri), CSF inflammation, infection, or neoplasm.
in its early stages is frequently asymptomatic. P
atients may complain of transient loss of vision lasting seconds ("transient obscurations of vision").
Initially VF exam reveals only a large blind spot
Treatment of papilledema depends on the cause.
2. Given the clinical presentation of any patient with chronic visual loss, be able to recognize:
a. Refractive errors
presbyopia occurs in later middle age as the eye loses its ability to accommodate.
Both eyes are affected, usually symmetrically.
The patient has trouble focusing at near and tends to hold targets further away
This is easily corrected with reading glasses or bifocals.
b. Cataracts
Opacity of the lens, usually associated with aging
The pupil may appear cloudy, white, or yellowish.
Patient complains of slowly progressive visual loss, glare, or washed-out colors.
Surgical extraction is considered when the patient's daily activities are affected by the cataractous visual loss.
A decreased red reflex may be appreciated when viewed through the direct ophthalmoscope held at a distance.
c. Glaucoma
damage to the optic nerve and visual field by elevated intraocular pressure
Open-angle glaucoma is more common in the elderly and results in painless progressive loss and contraction of peripheral visual field, sparing the central field until late in the disease.
Intraocular pressure increases because of decreased outflow of aqueous through the trabecular meshwork of the eye,
Increased pressure damages the retinal axons as they exit the eye at the optic disc
the optic disc may show cupping (an increased cup:disc ratio) or notching of the neural rim of the disc.
A cup larger than one half the size of the disc (cup:disc ratio >0.5) or asymmetry of the cup:disc ratios between the eyes should raise the suspicion of glaucomatous damage.
Treatment by an ophthalmologist may include medical, laser, or surgical intervention.
3. Given the clinical presentation of any patient with visual loss, be able to recognize when referral to an ophthalmologist is necessary for diagnosis.
TO BE ANNOUNCED
4. Given a patient with the chiasmal syndrome, be able to list the most common causes and the appropriate evaluation
caused by compression of the chiasm by a tumor, aneurysm, or other mass lesion.
One or both optic nerves or tracts are often involved.
This presents as slowly progressive visual loss in any age group.
Symptoms may range from none, to mild blurring in one or both eyes, to severe loss of vision.
The visual acuity may be normal or abnormal. T
VFs often demonstrate bitemporal VF loss respecting the vertical meridian (bitemporal hemianopia),
The optic discs may be normal or show optic atrophy.
MRI, are mandatory.
Thursday, February 21, 2008
LECTURE 2
LECTURE 2
1) Given a clinical presentation of a patient with a neurological complaint localize the pathology to the cortex, Sub cortex white/gray matter, brainstem, spinal cord, anterior horn cell, peripheral nerves, myoneural junction, or muscle.
AND SEE 2-9
2) Cortex
a) Stroke: Given a clinical presentation, recognize two types of strokes.
(1) Ischemic Stroke:
(a) caused by a lack of blood supply to part of the brain. T
(b) caused by atherosclerosis.
(c) Caused by blood clot can form on the plaque and block blood flow to the brain.
(i) This is a thrombotic stroke.
(2) Hemorrhagic Stroke:
(a) artery in the brain ruptures.
(b) Blood puts pressure on the surrounding brain tissue, causing edema.
(c) Brain cells beyond the rupture site become ischemic.
(i) Hypertension: The most common cause of a hemorrhagic stroke is high blood pressure.
1. The constant force of high blood pressure weakens blood vessel walls; this is typically in the basal ganglia or cerebellum.
(ii) Aneurysm leak: Another cause of a hemorrhagic stroke is leakage from an aneurysm
(iii) AV malformation: An uncommon cause of hemorrhage is rupture of an arteriovenous malformation. This group of congenitally malformed blood vessels can rupture.
Patients present with speech disturbances….aphasias.
Imaging: MRI
b) Aphasia: Given a clinical presentation, recognize expressive, receptive, conduction, transcortical motor, transcortical sensory, or anomic aphasia.
3) Subcortical White/Gray Matter disorders causing movement disorders: Given a clinical presentation, recognize chorea,
athetosis, tremor, dystonia, or tics.
v CHOREA: Rapid, irregular, relatively small amplitude, random-appearing rather continuous, non-stereotyped jerks or distal limbs.
Ø Non-repetitive or rhythmic brief muscle contractions
§ Huntington's disease
§ Sydenham's chorea
§ Tardive dyskinesia
Ø Hyperkinetic disorder
v ATHETOSIS: Wormlike, writhing, twisting movements of the limbs. They are slow
v TREMOR: Rhythmic, oscillatory movements, of the limbs, head, laryngeal muscles
Ø Essential
Ø Intention
Ø Hyperkinetic disorder
v DYSTONIA: Involuntary, sustained, patterned, and often repetitive muscle contractions of opposing muscles resulting in twisting, spasmodic or other abnormal postures
Ø Primary idiopathic
Ø Secondary
Ø Acute-drug induced
v TICS: Semi-involuntary, (often compulsive), repetitive, stereotyped movements
Ø . Motor tics: facial grimace, eye squint, head flip, etc.
§ Simple motor tic
§ Chronic motor tic
Ø Vocal tics: grunt, sniff, cough, snort, etc.
Ø Tourette syndrome
4) Brainstem: recognize crossed findings in brainstem lesions
CASE 5
right sided weakness and double vision.
left part of his mouth seemed drooped.
CAUSE OF CROSSED FINDINGS
Left lateral rectus palsy secondary to Cranial Nerve 6th nerve palsy.
Left pontine stroke presenting as a ventral pontine or “Millard-Gubler” syndrome
5) Spinal Cord: given a clinical presentation, recognize dorsal column disease, anterior spinal cord disease, and Brown-
Sequard syndrome, anterior horn cell disease, tabes dorsalis, and subacute combined degeneration.
· dorsal column disease: vibratory sense, proprioception, and deep pain (will be impaired?)
· anterior spinal cord disease: Loss of pain and temperature (+/- loss of corticospinals) with preservation of vibration and position sense specifically localizes to
· Brown-Sequard syndrome 9hemi-cord ): vibration and position sense are lost ipsilateral to the lesion, and pain and temperature sensation are lost contralateral to the lesion.
· anterior horn cell disease: SEE OBJ 6
· tabes dorsalis: is a manifestation of tertiary syphilis, where just the dorsal columns are affected.
· subacute combined degeneration: is the lesion of severe B12 deficiency, where both the dorsal columns and the corticospinal tracts (motor control descending from the cortex to the muscles) are impaired.
6) Anterior Horn Cell Diseases – recognize conditions primarily affecting this area.
Anterior Horn Cell diseases tend to be progressive and commonly at onset have upper and lower motor features. Fasciculations is a prominent clinical finding in these patients.
1. Poliomyelitis present with a spinal form as well as a brainstem form. The spinal form (most common) can occur with muscle pain and within 24 hrs the weakness reaches maximal intensity in the muscles involved. It involves the anterior horn cell area.
2. Amyotrophic Lateral Sclerosis (Lou Gehrig’s Disease) presents with progressive weakness, muscle twitching, and atrophy of the muscles.
CLIN PRESENT
A 3-day-old term infant has required Cesarean section at delivery because labor failed to progress. The infant has shown little spontaneous movement since birth, and has required intubation for respiratory failure. On examination, the infant has a "frog-leg" appearance, and absent deep tendon reflexes. Response to pin-prick is vigorous in all limbs. Prominent tongue fasciculation are noted, but otherwise the cranial nerves are normal.
Where is the lesion? Anterior Horn Cell (muscle biopsy showed changes consistent with neuropathic process. The condition is felt to be Spinal Muscular Atrophy).
7) Peripheral Nerve: Given a clinical presentation of a patient with sensory deficits, recognize peripheral neuropathy,
radiculopathy (spinal root lesion), mononeuropathy, diabetic neuropathy, combined system degeneration (B12 deficiency),
and carpal tunnel syndrome.
v Peripheral neuropathies are characterized by a "proximal-distal gradient", which means that the distal extremities are affected more than proximal extremities. This is called stocking-glove sensory loss.
v Peripheral sensory nerve disorders: Tingling, burning, and "pins and needles" complaints
Ø Diffuse distribution of these abnormal sensations (dysesthesias) suggests a systemic (i.e. diabetic) polyneuropathy. Local examples include
§ Compression of the median nerve causes dysesthesias of the thumb-half of palm. This is commonly caused by compression of the nerve in the bony tunnel of the wrist, called Carpal Tunnel Syndrome.
§ Compression of the radial nerve causes dysesthesias of the thumb-half of dorsum of hand and ulnar nerve compression causes dysesthesias on remaining half of palm and dorsum.
v Root lesions produce pain and sensory loss in a dermatomal distribution.
v Mononeuropathies have focal complaints and findings;
Ø polyneuropathies affect both sides of the body about equally.
Ø Carpal Tunnel Syndrome: injury to the median nerve as it passes through the carpel tunnel in the wrist. It can be caused by overuse of the wrist or other reasons why the nerve may thicken (hypothyroidism, amyloidosis, pregnancy).
Ø TInels and Phalen’s tests will be positive.
§ Tinel’s test is positive when shooting pain in the distribution of the median nerve is produced when the carpal tunnel is tapped.
· Phalen’s test is positive when the same pain is produced when the patient presses the dorsum of each hand against each other (therefore hyperflexing the wrist).
CLIN PRESENT:
A 25-year-old carpenter develops pain in his right forearm at night, and at work he notices that he cannot grip his hammer as strongly as before. On exam of the right upper extremity he has weakness of the right abductor pollicis brevis, and the finger flexors of the first and second digits. Loss of sensation in noted over the first two fingers of the right hand. His exam is otherwise normal. Where is the lesion? Peripheral Nerve (consistent with Carpal Tunnel Syndrome-mononeuropathy).
A 42-year-old woman arises from bed one morning and notes a tingling sensation in both legs that progresses over the day. By evening, she is unable to get out of bed. On examination she has absent reflexes in her legs, with trace reflexes in her arms. Both toes are down-going and her sensation is normal. She can barely move her legs but arm strength is normal. By the next morning she has lost all reflexes and is having trouble moving her arms. Where is the lesion? Peripheral Nerve (consistent with Guillain-Barre Syndrome – Polyradiculopathy)
8) Neuromuscular Junction: Given a clinical presentation, recognize myasthenia gravis.
Fatigability of the muscle is a hallmark of neuromuscular junction disease. Myasthenia gravis is the most common example of this type of lesion. Patients will report weakness getting worse with repetition, better with rest. The Electromyogram is diagnostic
CLIN PRESENT:
A 10-year-old boy with diabetes complains that over the past month he is very tired at the end of the day. He also has begun seeing double. On examination, he has bilateral ptosis, right greater than left, and he cannot adduct the left eye, nor elevate the right eye. He has mild symmetric proximal weakness, and he cannot close his eyes tightly.
9) Muscle: Given a clinical presentation, recognize myopathy.
Weakness tends to be proximal - patients have trouble rising from sitting, climbing stairs, reaching over their head). Pseudohypertrophy may be present, but atrophy is more common. Muscles may feel rubbery or doughy
Proximal symmetric weakness suggests a neuromuscular junction disorder or a myopathy.
10) Given the clinical presentation of a patient with altered awareness:
a) Determine whether the most likely cause of coma is metabolic-toxic or structural.
· structural lesions have focal features on the neurological examination
o has asymmetric findings.
· Examples of toxic-metabolic causes of coma include CNS-depressive drug overdosage, hyper- or hyponatremia, hypercalcemia, hepatic or renal encephalopathy, and hypoglycemia.
1. State of consciousness: Patients with metabolic problems often are less obtunded and may have waxing and waning of their arousal. Patients with acute structural lesions tend to stay at the same level of arousal or progressively deteriorate.
2. Respirations: Deep, rapid respirations are most commonly due to metabolic abnormalities.
3. Funduscopic examination: Papilledema usually indicates structural lesions. Papilledema does not occur in metabolic diseases except hypoparathyroidism, lead intoxication, and malignant hypertension.
4. Pupils: The pupils are usually symmetrical in coma from toxic-metabolic causes and asymmetric in structural causes.
Hypothermia may lead to fixed pupils, as does severe barbiturate intoxication. Neuromuscular blocking drugs produce midposition or small pupils.
5. Eye movements: Roving spontaneous eye movements with full excursion most often suggest metabolic-toxic disorders. Reflex eye movements are normally intact in toxic-metabolic coma, except rarely in phenobarbital or phenytoin intoxication or deep metabolic coma from other causes. Asymmetry in eye movement is a feature of structural lesions.
CLIN PRESENT
A 5-year-old boy is found unresponsive on the sidewalk. On exam there is no sign of trauma, but his pupils are equal, midposition and reactive. Both toes are upgoing and his DTRs are symmetric. Fundi are normal. He moves all limbs a little when stimulated. Which type of coma? Metabolic Coma.
b) Suggest the appropriate laboratory and radiographic evaluation.
1. Lumbar Puncture (LP): is indicated for the diagnosis of meningitis, subarachnoid hemorrhage, inflammatory diseases etc.
a. Red blood cells may be present in the collected CSF; this implies either a traumatic tap (common and an artifact of the collection process) or sub-arachnoid hemorrhage (very serious indicator of pathology).
b. marked decrease in the number of red blood cells from the first to the last tube collected (four are usually collected) usually indicates a traumatic tap.
2. CT: DXà alcohol-related syndromes
3. check serum B12 and thyroxine levels in any patient with dementia** B12 deficiency and hypothyroidism
4. electroencephalography (EEG) : To DX seizures à3 Hz spike and wave complexes
ALSO SEE OBJ 14.
c) Differentiate delirium from dementia and suggest the appropriate evaluation of dementia
d) Recognize alcohol-related dementia, normal pressure hydrocephalus (NPH), intracranial mass lesions (e.g., tumors and subdural hematoma), vitamin B12 deficiency, hypothyroidism, and neurosyphilis
· alcohol-related syndromes:
· normal pressure hydrocephalus (NPH): NPH is suggested in a patient with two or more characteristics of a classic triad: 1) Dementia, 2) Incontinence, and 3) Ataxia.
· intracranial mass lesions (e.g., tumors and subdural hematoma)
· B12 deficiency and hypothyroidism : may be suggested by their clinical syndromes, but it is wise to check serum B12 and thyroxine levels in any patient with dementia.
· neurosyphilis: presence of tabes dorsalis, Argyll-Robertson’s pupil, or cells and a positive VDRL in the CSF from a lumbar puncture.
11) Seizures: be able to characterize the seizure as tonic-clonic, absence, complex partial and simple partial
1) Tonic Clonic Seizures
a) The person may make a loud noise and fall to the floor
b) The body stiffens and the arms and legs begin to jerk rhythmically
c) Breathing may be shallow and irregular; skin may look blue
d) Bowel/bladder control may be lost
e) Excessive drooling may occur, and the tongue may be bitten
2) Absence Seizures
a) Loss of consciousness may last several minutes or even longer
b) Consciousness is regained slowly
c) Loss of consciousness is brief, 5-15 seconds
d) May look like daydreaming and be ignored
e) Associated with minor repetitive motions such as eye blinking or lip movements
f) Often there are 50-100 seizures a day
g) Immediate recovery of awareness
h) Occurs almost always in children and is often out grown
3) Simple Partial Seizures
a) Consciousness is not impaired.
b) The seizure may arise form any area of cortex with clinical manifestation depending on the site.
c) sensory seizures (flashing lights - occipital cortex, unusual odors - olfactory cortex), motor seizures (twitching of a limb or part of the face - motor cortex), or autonomic seizures (tachycardia - limbic system)
4) Complex Partial Seizure
a) most common type of focal seizures in both children and adults.
b) seizure may start with strange sensations (auras) such as fear, nausea, tingling.
c) Consciousness is impaired and the person may look dazed.
d) Repetitive movements are common, such as plucking at clothes, walking aimlessly or smacking of lips.
e) The vast majority last 1-5 minutes and are followed by drowsiness.
12) Headache: Given a clinical presentation, recognize:
1) Tension Headaches:
a) The headache is usually bilateral, frontal, occipital, or diffuse.
b) It tends to have gradual onset and may persist for days or even weeks.
c) The patient may describe a sensation of having a tight band around the head.
d) There may be mild nausea, but other associated symptoms are uncommon.
e) Many patients can identify stress as a precipitating factor.
f) The neurologic examination is normal, and many of these patients just want reassurance that their headaches are not a sign of a serious illness.
2) Musculoskeletal Headaches:
a) The pain usually begins in the neck, either unilateral or bilateral, and radiates forward to the occipital or frontal regions.
b) The headaches tend to last for days or weeks, and may be exacerbated by particular movements of the neck.
c) The neurologic examination is normal except for tenderness and spasm of the cervical spine and muscles.
3) Migraine Headaches:
a) occur more often in women than men,
b) Migraines may begin at any age, although the peak incidence is in the second and third decades.
c) About 2/3 of the patients have unilateral pain, with 1/3 being bilateral.
d) headache may be frontal, temporal, occipital or diffuse.
e) onset is usually over minutes or hours, with the duration 4 hours up to 3 days.
f) The most common associated symptoms include
i) nausea,
ii) vomiting
iii) visual disturbances, such as flashing lights or fortification scotoma.
g) The patient may also have a variety of transient neurologic complaints such as hemiparesis or decreased sensation on one side of the body in association with the headache.
h) In common migraine (Migraine without aura), the patient has headache and associated symptoms, but without focal neurologic complaints or findings.
i) In classic migraine (Migraine with aura), there are focal neurologic complaints or abnormalities on examination
i) such as ophthalmoplegia: associated with the headache.
ii) "prodrome" of a strange feeling or flashing lights, which heralds the onset of the headache by 15 to 45 minutes.
j) A minority of patients can identify a dietary factor such as chocolate, coffee, or alcohol, which precipitates the headaches.
k) Some patients will have a family history of similar headaches. Patients often complain of photophobia and phonophobia, so that they prefer to lie down in dark quite room when they get a headache.
l) Most patients will report that sleep will resolve the headache.
4) Cluster Headaches:
a) These are severe retroorbital headaches that occur almost exclusively in men.
b) The onset is usually in the 3rd or 4th decade, and the headaches occur several times a day or several times a week for several weeks or several months, followed by a remission which lasts for several months or several years.
c) Recurrent
d) unilateral,
e) Asociated with autonomic symptoms
i) rhinorrhea,
ii) excessive lacrimation
iii) conjunctival injection.
f) The headaches last for 15 minutes to 2 hours.
g) During the headaches the patient may be agitated, pace, or even bang his head against the wall.
h) This pain is so severe that many patients have considered suicide during the headache.
5) Subarachnoid Hemorrhage:
a) This headache has an instantaneous onset, often with associated loss of consciousness, and severe nausea and vomiting.
b) The patient comes to the emergency room and is either unconscious, or if awake, is completely disabled by a pain which is so severe that the patient cannot move.
c) There may be neck stiffness, generalized hyperreflexia, and upgoing toes.
d) An emergency CT scan of the head without contrast will show blood in the subarachnoid space.
e) emergency arteriogram to look for an aneurysm.
f) lumbar puncture may be done to look for red blood cells in the CSF if clinical suspicion is low.
6) Meningitis:
a) The headache usually begins over several hours or several days and is usually diffuse.
b) there may be associated fever or meningismus,
c) . Patients may have focal neurologic findings,
i) delirium
ii) lethargy,
d) CT or MRI scan of the head should be done if it is immediately available. In patients with a high level of suspicion for meningitis, do not wait several hours for an imaging procedure before proceeding with a lumbar puncture and instituting IV antibiotics.
7) Pseudotumor Cerebri (Idiopathic Intracranial Hypertension):
a) 95% of these patients are females, with the usual onset of headaches in the 3rd or 4th decade.
b) Patients are almost always markedly obese.
c) headaches tend to be dull, diffuse, with minimal associated symptoms
i) other than nausea and occasional episodes of visual disturbance (known as Transient Visual Obscurations).
d) headaches are gradual in onset and may last for weeks, months, or even years.
e) The neurologic examination is normal except for papilledema, with occasional visual field cut, particularly the nasal visual field.
f) Diagnostic studies include imaging of the head to exclude the presence of a structural lesion, and a lumbar puncture to document an increased (greater than 200 mm/H20) CSF pressure with otherwise normal spinal fluid.
8) Temporal Arteritis:
a) Patients have temporal, usually unilateral, headaches, which last for weeks or months. T
b) These are more often women than men and are usually over 60 years of age.
c) There may be a prodrome with weight loss, malaise, or a low-grade fever, all persisting for several weeks prior to the onset of headache.
d) Symptoms associated with the headache may include tenderness of the temporal artery, transient blurring of vision, jaw claudication (virtually pathognomonic), or muscle pain (in polymyalgia rheumatica).
e) The neurologic examination is usually normal except for possible scalp or temporal artery tenderness. Diagnostic studies to confirm the diagnosis include elevated sedimentation rate. A diagnosis of temporal arteritis is confirmed by a biopsy of the temporal artery, which is a relatively simple procedure.
9) Brain Tumor
a) occur at any age, and patients complain of gradual onset of focal or diffuse headache.
b) Increased intracranial pressure may result in nausea and vomiting, and patients may have a full range of neurologic complaints or abnormalities on examination.
c) Systemic symptoms such as weight loss or loss of appetite, or a history of previously diagnosed cancer, combined with focal neurologic complaints or findings, give a high probability for an intracranial tumor.
d) Diagnosis is made by cranial MR scanning, followed by brain biopsy.
13) Ataxia: Given a clinical presentation, recognize cerebellar, vestibular, or sensory ataxia.
Cerebellar ataxia is produced by lesions of the cerebellum itself or its afferent or efferent connections in the cerebellar peduncles, pons, or red nucleus.
Vestibular ataxia is produced by lesions anywhere along the peripheral eighth nerve pathway from labyrinth to brainstem and in the vestibular nuclei.
Sensory ataxia results from abnormalities anywhere along the afferent pathway from peripheral nerve, dorsal root, dorsal spinal tracts, or the sensory projection from the thalamus to the parietal lobe cortex. Most commonly the dorsal spinal tracts are the location but severe sensory neuropathy can also cause ataxia.
14) Given a clinical presentation, recognize when the following procedures are indicated and how to interpret their results:
a) Electroencephalogram: Seizure
b) Lumbar Puncture : Infection, low suspicion for subarachnoid hemorrhage.
c) Head CT : Tumor, hemorrhage
d) Head MRI : Tumor
e) Temporal artery biopsy : Temporal Arteritis.
1) Given a clinical presentation of a patient with a neurological complaint localize the pathology to the cortex, Sub cortex white/gray matter, brainstem, spinal cord, anterior horn cell, peripheral nerves, myoneural junction, or muscle.
AND SEE 2-9
2) Cortex
a) Stroke: Given a clinical presentation, recognize two types of strokes.
(1) Ischemic Stroke:
(a) caused by a lack of blood supply to part of the brain. T
(b) caused by atherosclerosis.
(c) Caused by blood clot can form on the plaque and block blood flow to the brain.
(i) This is a thrombotic stroke.
(2) Hemorrhagic Stroke:
(a) artery in the brain ruptures.
(b) Blood puts pressure on the surrounding brain tissue, causing edema.
(c) Brain cells beyond the rupture site become ischemic.
(i) Hypertension: The most common cause of a hemorrhagic stroke is high blood pressure.
1. The constant force of high blood pressure weakens blood vessel walls; this is typically in the basal ganglia or cerebellum.
(ii) Aneurysm leak: Another cause of a hemorrhagic stroke is leakage from an aneurysm
(iii) AV malformation: An uncommon cause of hemorrhage is rupture of an arteriovenous malformation. This group of congenitally malformed blood vessels can rupture.
Patients present with speech disturbances….aphasias.
Imaging: MRI
b) Aphasia: Given a clinical presentation, recognize expressive, receptive, conduction, transcortical motor, transcortical sensory, or anomic aphasia.
3) Subcortical White/Gray Matter disorders causing movement disorders: Given a clinical presentation, recognize chorea,
athetosis, tremor, dystonia, or tics.
v CHOREA: Rapid, irregular, relatively small amplitude, random-appearing rather continuous, non-stereotyped jerks or distal limbs.
Ø Non-repetitive or rhythmic brief muscle contractions
§ Huntington's disease
§ Sydenham's chorea
§ Tardive dyskinesia
Ø Hyperkinetic disorder
v ATHETOSIS: Wormlike, writhing, twisting movements of the limbs. They are slow
v TREMOR: Rhythmic, oscillatory movements, of the limbs, head, laryngeal muscles
Ø Essential
Ø Intention
Ø Hyperkinetic disorder
v DYSTONIA: Involuntary, sustained, patterned, and often repetitive muscle contractions of opposing muscles resulting in twisting, spasmodic or other abnormal postures
Ø Primary idiopathic
Ø Secondary
Ø Acute-drug induced
v TICS: Semi-involuntary, (often compulsive), repetitive, stereotyped movements
Ø . Motor tics: facial grimace, eye squint, head flip, etc.
§ Simple motor tic
§ Chronic motor tic
Ø Vocal tics: grunt, sniff, cough, snort, etc.
Ø Tourette syndrome
4) Brainstem: recognize crossed findings in brainstem lesions
CASE 5
right sided weakness and double vision.
left part of his mouth seemed drooped.
CAUSE OF CROSSED FINDINGS
Left lateral rectus palsy secondary to Cranial Nerve 6th nerve palsy.
Left pontine stroke presenting as a ventral pontine or “Millard-Gubler” syndrome
5) Spinal Cord: given a clinical presentation, recognize dorsal column disease, anterior spinal cord disease, and Brown-
Sequard syndrome, anterior horn cell disease, tabes dorsalis, and subacute combined degeneration.
· dorsal column disease: vibratory sense, proprioception, and deep pain (will be impaired?)
· anterior spinal cord disease: Loss of pain and temperature (+/- loss of corticospinals) with preservation of vibration and position sense specifically localizes to
· Brown-Sequard syndrome 9hemi-cord ): vibration and position sense are lost ipsilateral to the lesion, and pain and temperature sensation are lost contralateral to the lesion.
· anterior horn cell disease: SEE OBJ 6
· tabes dorsalis: is a manifestation of tertiary syphilis, where just the dorsal columns are affected.
· subacute combined degeneration: is the lesion of severe B12 deficiency, where both the dorsal columns and the corticospinal tracts (motor control descending from the cortex to the muscles) are impaired.
6) Anterior Horn Cell Diseases – recognize conditions primarily affecting this area.
Anterior Horn Cell diseases tend to be progressive and commonly at onset have upper and lower motor features. Fasciculations is a prominent clinical finding in these patients.
1. Poliomyelitis present with a spinal form as well as a brainstem form. The spinal form (most common) can occur with muscle pain and within 24 hrs the weakness reaches maximal intensity in the muscles involved. It involves the anterior horn cell area.
2. Amyotrophic Lateral Sclerosis (Lou Gehrig’s Disease) presents with progressive weakness, muscle twitching, and atrophy of the muscles.
CLIN PRESENT
A 3-day-old term infant has required Cesarean section at delivery because labor failed to progress. The infant has shown little spontaneous movement since birth, and has required intubation for respiratory failure. On examination, the infant has a "frog-leg" appearance, and absent deep tendon reflexes. Response to pin-prick is vigorous in all limbs. Prominent tongue fasciculation are noted, but otherwise the cranial nerves are normal.
Where is the lesion? Anterior Horn Cell (muscle biopsy showed changes consistent with neuropathic process. The condition is felt to be Spinal Muscular Atrophy).
7) Peripheral Nerve: Given a clinical presentation of a patient with sensory deficits, recognize peripheral neuropathy,
radiculopathy (spinal root lesion), mononeuropathy, diabetic neuropathy, combined system degeneration (B12 deficiency),
and carpal tunnel syndrome.
v Peripheral neuropathies are characterized by a "proximal-distal gradient", which means that the distal extremities are affected more than proximal extremities. This is called stocking-glove sensory loss.
v Peripheral sensory nerve disorders: Tingling, burning, and "pins and needles" complaints
Ø Diffuse distribution of these abnormal sensations (dysesthesias) suggests a systemic (i.e. diabetic) polyneuropathy. Local examples include
§ Compression of the median nerve causes dysesthesias of the thumb-half of palm. This is commonly caused by compression of the nerve in the bony tunnel of the wrist, called Carpal Tunnel Syndrome.
§ Compression of the radial nerve causes dysesthesias of the thumb-half of dorsum of hand and ulnar nerve compression causes dysesthesias on remaining half of palm and dorsum.
v Root lesions produce pain and sensory loss in a dermatomal distribution.
v Mononeuropathies have focal complaints and findings;
Ø polyneuropathies affect both sides of the body about equally.
Ø Carpal Tunnel Syndrome: injury to the median nerve as it passes through the carpel tunnel in the wrist. It can be caused by overuse of the wrist or other reasons why the nerve may thicken (hypothyroidism, amyloidosis, pregnancy).
Ø TInels and Phalen’s tests will be positive.
§ Tinel’s test is positive when shooting pain in the distribution of the median nerve is produced when the carpal tunnel is tapped.
· Phalen’s test is positive when the same pain is produced when the patient presses the dorsum of each hand against each other (therefore hyperflexing the wrist).
CLIN PRESENT:
A 25-year-old carpenter develops pain in his right forearm at night, and at work he notices that he cannot grip his hammer as strongly as before. On exam of the right upper extremity he has weakness of the right abductor pollicis brevis, and the finger flexors of the first and second digits. Loss of sensation in noted over the first two fingers of the right hand. His exam is otherwise normal. Where is the lesion? Peripheral Nerve (consistent with Carpal Tunnel Syndrome-mononeuropathy).
A 42-year-old woman arises from bed one morning and notes a tingling sensation in both legs that progresses over the day. By evening, she is unable to get out of bed. On examination she has absent reflexes in her legs, with trace reflexes in her arms. Both toes are down-going and her sensation is normal. She can barely move her legs but arm strength is normal. By the next morning she has lost all reflexes and is having trouble moving her arms. Where is the lesion? Peripheral Nerve (consistent with Guillain-Barre Syndrome – Polyradiculopathy)
8) Neuromuscular Junction: Given a clinical presentation, recognize myasthenia gravis.
Fatigability of the muscle is a hallmark of neuromuscular junction disease. Myasthenia gravis is the most common example of this type of lesion. Patients will report weakness getting worse with repetition, better with rest. The Electromyogram is diagnostic
CLIN PRESENT:
A 10-year-old boy with diabetes complains that over the past month he is very tired at the end of the day. He also has begun seeing double. On examination, he has bilateral ptosis, right greater than left, and he cannot adduct the left eye, nor elevate the right eye. He has mild symmetric proximal weakness, and he cannot close his eyes tightly.
9) Muscle: Given a clinical presentation, recognize myopathy.
Weakness tends to be proximal - patients have trouble rising from sitting, climbing stairs, reaching over their head). Pseudohypertrophy may be present, but atrophy is more common. Muscles may feel rubbery or doughy
Proximal symmetric weakness suggests a neuromuscular junction disorder or a myopathy.
10) Given the clinical presentation of a patient with altered awareness:
a) Determine whether the most likely cause of coma is metabolic-toxic or structural.
· structural lesions have focal features on the neurological examination
o has asymmetric findings.
· Examples of toxic-metabolic causes of coma include CNS-depressive drug overdosage, hyper- or hyponatremia, hypercalcemia, hepatic or renal encephalopathy, and hypoglycemia.
1. State of consciousness: Patients with metabolic problems often are less obtunded and may have waxing and waning of their arousal. Patients with acute structural lesions tend to stay at the same level of arousal or progressively deteriorate.
2. Respirations: Deep, rapid respirations are most commonly due to metabolic abnormalities.
3. Funduscopic examination: Papilledema usually indicates structural lesions. Papilledema does not occur in metabolic diseases except hypoparathyroidism, lead intoxication, and malignant hypertension.
4. Pupils: The pupils are usually symmetrical in coma from toxic-metabolic causes and asymmetric in structural causes.
Hypothermia may lead to fixed pupils, as does severe barbiturate intoxication. Neuromuscular blocking drugs produce midposition or small pupils.
5. Eye movements: Roving spontaneous eye movements with full excursion most often suggest metabolic-toxic disorders. Reflex eye movements are normally intact in toxic-metabolic coma, except rarely in phenobarbital or phenytoin intoxication or deep metabolic coma from other causes. Asymmetry in eye movement is a feature of structural lesions.
CLIN PRESENT
A 5-year-old boy is found unresponsive on the sidewalk. On exam there is no sign of trauma, but his pupils are equal, midposition and reactive. Both toes are upgoing and his DTRs are symmetric. Fundi are normal. He moves all limbs a little when stimulated. Which type of coma? Metabolic Coma.
b) Suggest the appropriate laboratory and radiographic evaluation.
1. Lumbar Puncture (LP): is indicated for the diagnosis of meningitis, subarachnoid hemorrhage, inflammatory diseases etc.
a. Red blood cells may be present in the collected CSF; this implies either a traumatic tap (common and an artifact of the collection process) or sub-arachnoid hemorrhage (very serious indicator of pathology).
b. marked decrease in the number of red blood cells from the first to the last tube collected (four are usually collected) usually indicates a traumatic tap.
2. CT: DXà alcohol-related syndromes
3. check serum B12 and thyroxine levels in any patient with dementia** B12 deficiency and hypothyroidism
4. electroencephalography (EEG) : To DX seizures à3 Hz spike and wave complexes
ALSO SEE OBJ 14.
c) Differentiate delirium from dementia and suggest the appropriate evaluation of dementia
d) Recognize alcohol-related dementia, normal pressure hydrocephalus (NPH), intracranial mass lesions (e.g., tumors and subdural hematoma), vitamin B12 deficiency, hypothyroidism, and neurosyphilis
· alcohol-related syndromes:
· normal pressure hydrocephalus (NPH): NPH is suggested in a patient with two or more characteristics of a classic triad: 1) Dementia, 2) Incontinence, and 3) Ataxia.
· intracranial mass lesions (e.g., tumors and subdural hematoma)
· B12 deficiency and hypothyroidism : may be suggested by their clinical syndromes, but it is wise to check serum B12 and thyroxine levels in any patient with dementia.
· neurosyphilis: presence of tabes dorsalis, Argyll-Robertson’s pupil, or cells and a positive VDRL in the CSF from a lumbar puncture.
11) Seizures: be able to characterize the seizure as tonic-clonic, absence, complex partial and simple partial
1) Tonic Clonic Seizures
a) The person may make a loud noise and fall to the floor
b) The body stiffens and the arms and legs begin to jerk rhythmically
c) Breathing may be shallow and irregular; skin may look blue
d) Bowel/bladder control may be lost
e) Excessive drooling may occur, and the tongue may be bitten
2) Absence Seizures
a) Loss of consciousness may last several minutes or even longer
b) Consciousness is regained slowly
c) Loss of consciousness is brief, 5-15 seconds
d) May look like daydreaming and be ignored
e) Associated with minor repetitive motions such as eye blinking or lip movements
f) Often there are 50-100 seizures a day
g) Immediate recovery of awareness
h) Occurs almost always in children and is often out grown
3) Simple Partial Seizures
a) Consciousness is not impaired.
b) The seizure may arise form any area of cortex with clinical manifestation depending on the site.
c) sensory seizures (flashing lights - occipital cortex, unusual odors - olfactory cortex), motor seizures (twitching of a limb or part of the face - motor cortex), or autonomic seizures (tachycardia - limbic system)
4) Complex Partial Seizure
a) most common type of focal seizures in both children and adults.
b) seizure may start with strange sensations (auras) such as fear, nausea, tingling.
c) Consciousness is impaired and the person may look dazed.
d) Repetitive movements are common, such as plucking at clothes, walking aimlessly or smacking of lips.
e) The vast majority last 1-5 minutes and are followed by drowsiness.
12) Headache: Given a clinical presentation, recognize:
1) Tension Headaches:
a) The headache is usually bilateral, frontal, occipital, or diffuse.
b) It tends to have gradual onset and may persist for days or even weeks.
c) The patient may describe a sensation of having a tight band around the head.
d) There may be mild nausea, but other associated symptoms are uncommon.
e) Many patients can identify stress as a precipitating factor.
f) The neurologic examination is normal, and many of these patients just want reassurance that their headaches are not a sign of a serious illness.
2) Musculoskeletal Headaches:
a) The pain usually begins in the neck, either unilateral or bilateral, and radiates forward to the occipital or frontal regions.
b) The headaches tend to last for days or weeks, and may be exacerbated by particular movements of the neck.
c) The neurologic examination is normal except for tenderness and spasm of the cervical spine and muscles.
3) Migraine Headaches:
a) occur more often in women than men,
b) Migraines may begin at any age, although the peak incidence is in the second and third decades.
c) About 2/3 of the patients have unilateral pain, with 1/3 being bilateral.
d) headache may be frontal, temporal, occipital or diffuse.
e) onset is usually over minutes or hours, with the duration 4 hours up to 3 days.
f) The most common associated symptoms include
i) nausea,
ii) vomiting
iii) visual disturbances, such as flashing lights or fortification scotoma.
g) The patient may also have a variety of transient neurologic complaints such as hemiparesis or decreased sensation on one side of the body in association with the headache.
h) In common migraine (Migraine without aura), the patient has headache and associated symptoms, but without focal neurologic complaints or findings.
i) In classic migraine (Migraine with aura), there are focal neurologic complaints or abnormalities on examination
i) such as ophthalmoplegia: associated with the headache.
ii) "prodrome" of a strange feeling or flashing lights, which heralds the onset of the headache by 15 to 45 minutes.
j) A minority of patients can identify a dietary factor such as chocolate, coffee, or alcohol, which precipitates the headaches.
k) Some patients will have a family history of similar headaches. Patients often complain of photophobia and phonophobia, so that they prefer to lie down in dark quite room when they get a headache.
l) Most patients will report that sleep will resolve the headache.
4) Cluster Headaches:
a) These are severe retroorbital headaches that occur almost exclusively in men.
b) The onset is usually in the 3rd or 4th decade, and the headaches occur several times a day or several times a week for several weeks or several months, followed by a remission which lasts for several months or several years.
c) Recurrent
d) unilateral,
e) Asociated with autonomic symptoms
i) rhinorrhea,
ii) excessive lacrimation
iii) conjunctival injection.
f) The headaches last for 15 minutes to 2 hours.
g) During the headaches the patient may be agitated, pace, or even bang his head against the wall.
h) This pain is so severe that many patients have considered suicide during the headache.
5) Subarachnoid Hemorrhage:
a) This headache has an instantaneous onset, often with associated loss of consciousness, and severe nausea and vomiting.
b) The patient comes to the emergency room and is either unconscious, or if awake, is completely disabled by a pain which is so severe that the patient cannot move.
c) There may be neck stiffness, generalized hyperreflexia, and upgoing toes.
d) An emergency CT scan of the head without contrast will show blood in the subarachnoid space.
e) emergency arteriogram to look for an aneurysm.
f) lumbar puncture may be done to look for red blood cells in the CSF if clinical suspicion is low.
6) Meningitis:
a) The headache usually begins over several hours or several days and is usually diffuse.
b) there may be associated fever or meningismus,
c) . Patients may have focal neurologic findings,
i) delirium
ii) lethargy,
d) CT or MRI scan of the head should be done if it is immediately available. In patients with a high level of suspicion for meningitis, do not wait several hours for an imaging procedure before proceeding with a lumbar puncture and instituting IV antibiotics.
7) Pseudotumor Cerebri (Idiopathic Intracranial Hypertension):
a) 95% of these patients are females, with the usual onset of headaches in the 3rd or 4th decade.
b) Patients are almost always markedly obese.
c) headaches tend to be dull, diffuse, with minimal associated symptoms
i) other than nausea and occasional episodes of visual disturbance (known as Transient Visual Obscurations).
d) headaches are gradual in onset and may last for weeks, months, or even years.
e) The neurologic examination is normal except for papilledema, with occasional visual field cut, particularly the nasal visual field.
f) Diagnostic studies include imaging of the head to exclude the presence of a structural lesion, and a lumbar puncture to document an increased (greater than 200 mm/H20) CSF pressure with otherwise normal spinal fluid.
8) Temporal Arteritis:
a) Patients have temporal, usually unilateral, headaches, which last for weeks or months. T
b) These are more often women than men and are usually over 60 years of age.
c) There may be a prodrome with weight loss, malaise, or a low-grade fever, all persisting for several weeks prior to the onset of headache.
d) Symptoms associated with the headache may include tenderness of the temporal artery, transient blurring of vision, jaw claudication (virtually pathognomonic), or muscle pain (in polymyalgia rheumatica).
e) The neurologic examination is usually normal except for possible scalp or temporal artery tenderness. Diagnostic studies to confirm the diagnosis include elevated sedimentation rate. A diagnosis of temporal arteritis is confirmed by a biopsy of the temporal artery, which is a relatively simple procedure.
9) Brain Tumor
a) occur at any age, and patients complain of gradual onset of focal or diffuse headache.
b) Increased intracranial pressure may result in nausea and vomiting, and patients may have a full range of neurologic complaints or abnormalities on examination.
c) Systemic symptoms such as weight loss or loss of appetite, or a history of previously diagnosed cancer, combined with focal neurologic complaints or findings, give a high probability for an intracranial tumor.
d) Diagnosis is made by cranial MR scanning, followed by brain biopsy.
13) Ataxia: Given a clinical presentation, recognize cerebellar, vestibular, or sensory ataxia.
Cerebellar ataxia is produced by lesions of the cerebellum itself or its afferent or efferent connections in the cerebellar peduncles, pons, or red nucleus.
Vestibular ataxia is produced by lesions anywhere along the peripheral eighth nerve pathway from labyrinth to brainstem and in the vestibular nuclei.
Sensory ataxia results from abnormalities anywhere along the afferent pathway from peripheral nerve, dorsal root, dorsal spinal tracts, or the sensory projection from the thalamus to the parietal lobe cortex. Most commonly the dorsal spinal tracts are the location but severe sensory neuropathy can also cause ataxia.
14) Given a clinical presentation, recognize when the following procedures are indicated and how to interpret their results:
a) Electroencephalogram: Seizure
b) Lumbar Puncture : Infection, low suspicion for subarachnoid hemorrhage.
c) Head CT : Tumor, hemorrhage
d) Head MRI : Tumor
e) Temporal artery biopsy : Temporal Arteritis.
LECTURE 5
1. Given a patient with memory loss, recognize when the most likley diagnosis is Mild Cognitive Impairment (MCI), Alzheimer's Disease (AD), Vascular Dementia (VD), Frontotemporal lobe dysfunction , Lewy Body disease, Pesuedodementia, Creutzfeldt Jacob disease (CJD).
MCI
-Isolated memory impairment with other domains spared fo 1 or more years
-15% of patients progress to probably AD each year with 80% progressing in 6 years
AD
See objective 4
VD
-history of clinical strokes with a sudden onset with stepwise progression and lateralized findings
Frontotemporal lobe dysfunction (FTD, Pick's DZ primary progressive aphasia, semantic dementia)
-Presents at a younger age usually less than 65
Lewy Body Dementia
-difficult to separate from AD
-Early visual hallucinations
-parkinsonism, fluctuating cognition, REM behavioral disorder
Pseudodementia
-Depression is prominant
-no sundowning
-neuropsych testing deficits not severe
-many elderly patients with pseudodementia develop AD
CJD
-Rapid progression of dementia(fatal in 1 yr)
-myoclonus
-abnormal EEG
-visuoperceptive derangements
-CSF positive for 14-3-3
2. Given a patient with dementia, recognize when a patient has a potentially reversible cause.
Metabolic Disorders (can be tested for by lab screens)
B12 deficiency
Thyroid disease
Folate deficieny
Infectious Causes (culture etc.)
Syphilis
Crytococcal meningitis
3. Given the clinical presentation of a patient with dementia, recognize aphasia, apraxia, agnosia, and disturbances in executive function.
Aphasia
Broad term encompassing language deficits. Includes Anomia(difficulty naming things), word finding, comprehension deficiencies (wernicke and transcortical sensory aphasia), and expression deficiencies( brochas and transcortical motor aphasia)
Apraxia
The loss of ability to perform a learned motor task despite intact basic sensory and motor function.
Types
Ideomotor: cannot pantomime gestures to command
Ideational: cannot sequence acts of a multi-step complex action
Conceptual: loss of semantic knowledge involving tool use
Others include Dressing/construction/gait
Agnosia
Difficulty recognizing objects not just names. Prosopagnosia is a difficulty recognizing faces.
Executive function
Problems with planing, organizing, and goal oriented behavior.
Manifestations
a) trouble with check book balancing or paying bills
b) cannot prepare a large meal with several dishes
c) cannot keep house clean
d) cannot keep up with job
e) cannot complete tasks
f) perseveration (Persistent repetition of an activity, word, phrase, or movement, such as tapping, wiping, and picking.)
4. Given the clinical presentation of a patient with Alzheimer's Disease, make the appropriate diagnosis by using the NINCDS-ADRDA and DSM-IV criteria
NINCDS-ADRDA
Probable AD
-Dementia confirmed by MSE and Neurphycologic Testing.
-Deficits in at least 2 cognitive domains.
-Progressive cognitive decline.
-Normal consciousness(No delerium).
-No other explanation for symptoms.
Possible AD (When something from the list below prevents patient from meeting probable AD)
-Dementia with atypical onset/course without another explanation.
-Presence of another disease process capable of causing dementia but not the likely cause of -dementia.
-Progressive deterioration of 1 cognitive domain.
Definite AD
Probable AD with Autopsy evidence.
DSM IV
Multiple cognitive deficits including
1) memory impairment
2) and one or more of the following
-Aphasia
-Apraxia
-Agnosia
-Executive Functions
Signs Pointing Towards AD
-Deficits cause significant impairment in social and occupational settings. There is a gradual onset with continuing decline. Deficits are not attributable to other condition or substance.
Signs Pointing Against AD
-Rapid onset. Focal sensorimotor signs. Seizures or gait issues early in the disease process.
Clinical Presentation of AD
-Memory loss is the 1st thing to go (Forming new memories is impaired while recall of old memories is still intact)
-Anomia is the initial language deficit, then comes comprehension, then comes empty speech.
-Problems with perception first include easily becoming lost in new surroundings, and progressively worsen to becoming lost/confused in own home.
-Apraxia and Executive function issues also are commonly seen.
-A majority of patients with AD often have behavioral symptoms including Apathy, Irritability, and Delusions. Delusions include phantom border, paranoia, and occasionally capgras syndrome.
5. Given the clinical presentation of a patient with a movement disorder, recognize parkinson's disease and Huntington's chorea.
Parkinson's DZ
Disorder of the Basal Ganglia with a loss of dopaminergic cells in the substantia nigra.
4 Cardinal Features
1)Resting Tremor
-4-7hz in limbs, jaw, face, tongue
-postural tremor
2) Rigidity
-Resistance to passive movement. May be seen in cogwheel fashion
3) Bradykinesia/Hypokinesia
a) masked facies. decreased eye blinking
b) lack of fidgeting at rest
c) purposeful activity is slow
d) drooling (b/c bad swallowing)
e) cant roll over in bed
f) slowed and low amplitude alternating movements
4)Posture
- decrease in stride length
- shuffling gait
- festination
- tendency to fall especially backwards
Other findings:
-eczema of the forehead
-constipation is often the very first sign preceeding everything else
-responsive to L-DOPA
-Tendency to act out dreams
-Depression
Huntington's Chorea
-Genetic defect with CAG repeats on Chromosome 4.
-Caudate and putamen are atrophic
Clinical Features (each of these are possible manifestations):
-Onset in the 4th/5th decade of life. 1/2 of the patients present with movement disorder(choreoathetosis, and much less commonly parkinsonism) and 1/2 of the patients present with psychiatric disorder
1) Choreoathetosis
-Chorea (jerky coarse movements)
-Athetosis(slow writhing movements)
-Gait(lurching, Dance-like)
2) Dementia(Frontal subcortical)
-executive impairment
-decreased concentration and attention
-memory problems due to poor retreival (unlike AD which is a storage problem)
-poor speech
3)Psychiatric
-Personality changes
-Depression/Bipolar
-Anxiety
-Psychosis
-Suicidal
4) Dysarthria/Dysphagia
5) cannot maintain portruded tongue
WESTPHAL VARIANT has parkinsonism and not choreathetosis and is juvenile onset.
6. List the differential diagnosis for Parkinson's disease and Huntington's chorea.
Parkinson's Disease Differential
Parkinsonisum Plus Syndromes
-Don't respond to L-DOPA
1)Progressive Supranuclear Palsy
-early falls
-progerssive paralysis of voluntary eye movements. development of downgaze paresis
-oculovestibular responses stay intact
-Hummingbird sign in MRI
2)Multiple System Atrophy
a. Striatonigral Degeneration-Pyramidal Dysfunction
b. Olivopontocerebellar atrophy-Cerebellar Dysfunction
c. Shy Drager syndrome-Autonomic Dysfunction (including sever orthostatic hypotension)
3)Corticobasal degeneration
-Asymmetric motor findings
-Terrible Limb Apraxia
-Alien limb (autonomous behavior of a hand or arm)
Drug induced
-Neuroleptics (common)
-Metoclopromide (common)
-alpha-methyldopa
-reserpine
-Amiodarone
Toxic
-Cyanide
-Carbon Monoxide(bilateral pallidal necrosis on imaging)
-Manganese intoxication (seen commonly with liver cirrohsis, seen in welders, bright signal in basal ganglia on T1 MRI)
Wilson's Dz
-Copper metabolism screwed up
-Kayser-Fleischer Rings
-serum ceruloplasmin down urinary copper up
-liver disease
Focal Lesions
-vascular,neoplastic, and infectious lesions that can be detected on imaging)
Huntington's DZ Differential
Sydenham's Chorea
1) Post streptococcal
2) seen in conjunction with rheumatic fecer
3) ASO positive
4)self-limited
Chorea Gravidarum (Birth control Chorea)
-Caused by estrogen, with prior sydenham's chorea as a risk factor
Hyperthyroidism
Tardive Dyskinesia
-Prior neuroleptic use
-This is a real question b/c many have prior psych dz and have taken neuroleptics, which can be confused with Huntingtons
-Tardive Dyskinesia patients can hold their tongue in protrusion whil Huntingtons patients cannot
Wilson's Dz
-See parkinsons differential
Senile Chorea
-onset >60y/o
-No neuropsychiatric symptoms
Drugs
-Birth control
-L-dopa and other Dopamine agonists
-Stimulants
-Phenytoin
-Carbamazepine
-Ethosuximide
MCI
-Isolated memory impairment with other domains spared fo 1 or more years
-15% of patients progress to probably AD each year with 80% progressing in 6 years
AD
See objective 4
VD
-history of clinical strokes with a sudden onset with stepwise progression and lateralized findings
Frontotemporal lobe dysfunction (FTD, Pick's DZ primary progressive aphasia, semantic dementia)
-Presents at a younger age usually less than 65
Lewy Body Dementia
-difficult to separate from AD
-Early visual hallucinations
-parkinsonism, fluctuating cognition, REM behavioral disorder
Pseudodementia
-Depression is prominant
-no sundowning
-neuropsych testing deficits not severe
-many elderly patients with pseudodementia develop AD
CJD
-Rapid progression of dementia(fatal in 1 yr)
-myoclonus
-abnormal EEG
-visuoperceptive derangements
-CSF positive for 14-3-3
2. Given a patient with dementia, recognize when a patient has a potentially reversible cause.
Metabolic Disorders (can be tested for by lab screens)
B12 deficiency
Thyroid disease
Folate deficieny
Infectious Causes (culture etc.)
Syphilis
Crytococcal meningitis
3. Given the clinical presentation of a patient with dementia, recognize aphasia, apraxia, agnosia, and disturbances in executive function.
Aphasia
Broad term encompassing language deficits. Includes Anomia(difficulty naming things), word finding, comprehension deficiencies (wernicke and transcortical sensory aphasia), and expression deficiencies( brochas and transcortical motor aphasia)
Apraxia
The loss of ability to perform a learned motor task despite intact basic sensory and motor function.
Types
Ideomotor: cannot pantomime gestures to command
Ideational: cannot sequence acts of a multi-step complex action
Conceptual: loss of semantic knowledge involving tool use
Others include Dressing/construction/gait
Agnosia
Difficulty recognizing objects not just names. Prosopagnosia is a difficulty recognizing faces.
Executive function
Problems with planing, organizing, and goal oriented behavior.
Manifestations
a) trouble with check book balancing or paying bills
b) cannot prepare a large meal with several dishes
c) cannot keep house clean
d) cannot keep up with job
e) cannot complete tasks
f) perseveration (Persistent repetition of an activity, word, phrase, or movement, such as tapping, wiping, and picking.)
4. Given the clinical presentation of a patient with Alzheimer's Disease, make the appropriate diagnosis by using the NINCDS-ADRDA and DSM-IV criteria
NINCDS-ADRDA
Probable AD
-Dementia confirmed by MSE and Neurphycologic Testing.
-Deficits in at least 2 cognitive domains.
-Progressive cognitive decline.
-Normal consciousness(No delerium).
-No other explanation for symptoms.
Possible AD (When something from the list below prevents patient from meeting probable AD)
-Dementia with atypical onset/course without another explanation.
-Presence of another disease process capable of causing dementia but not the likely cause of -dementia.
-Progressive deterioration of 1 cognitive domain.
Definite AD
Probable AD with Autopsy evidence.
DSM IV
Multiple cognitive deficits including
1) memory impairment
2) and one or more of the following
-Aphasia
-Apraxia
-Agnosia
-Executive Functions
Signs Pointing Towards AD
-Deficits cause significant impairment in social and occupational settings. There is a gradual onset with continuing decline. Deficits are not attributable to other condition or substance.
Signs Pointing Against AD
-Rapid onset. Focal sensorimotor signs. Seizures or gait issues early in the disease process.
Clinical Presentation of AD
-Memory loss is the 1st thing to go (Forming new memories is impaired while recall of old memories is still intact)
-Anomia is the initial language deficit, then comes comprehension, then comes empty speech.
-Problems with perception first include easily becoming lost in new surroundings, and progressively worsen to becoming lost/confused in own home.
-Apraxia and Executive function issues also are commonly seen.
-A majority of patients with AD often have behavioral symptoms including Apathy, Irritability, and Delusions. Delusions include phantom border, paranoia, and occasionally capgras syndrome.
5. Given the clinical presentation of a patient with a movement disorder, recognize parkinson's disease and Huntington's chorea.
Parkinson's DZ
Disorder of the Basal Ganglia with a loss of dopaminergic cells in the substantia nigra.
4 Cardinal Features
1)Resting Tremor
-4-7hz in limbs, jaw, face, tongue
-postural tremor
2) Rigidity
-Resistance to passive movement. May be seen in cogwheel fashion
3) Bradykinesia/Hypokinesia
a) masked facies. decreased eye blinking
b) lack of fidgeting at rest
c) purposeful activity is slow
d) drooling (b/c bad swallowing)
e) cant roll over in bed
f) slowed and low amplitude alternating movements
4)Posture
- decrease in stride length
- shuffling gait
- festination
- tendency to fall especially backwards
Other findings:
-eczema of the forehead
-constipation is often the very first sign preceeding everything else
-responsive to L-DOPA
-Tendency to act out dreams
-Depression
Huntington's Chorea
-Genetic defect with CAG repeats on Chromosome 4.
-Caudate and putamen are atrophic
Clinical Features (each of these are possible manifestations):
-Onset in the 4th/5th decade of life. 1/2 of the patients present with movement disorder(choreoathetosis, and much less commonly parkinsonism) and 1/2 of the patients present with psychiatric disorder
1) Choreoathetosis
-Chorea (jerky coarse movements)
-Athetosis(slow writhing movements)
-Gait(lurching, Dance-like)
2) Dementia(Frontal subcortical)
-executive impairment
-decreased concentration and attention
-memory problems due to poor retreival (unlike AD which is a storage problem)
-poor speech
3)Psychiatric
-Personality changes
-Depression/Bipolar
-Anxiety
-Psychosis
-Suicidal
4) Dysarthria/Dysphagia
5) cannot maintain portruded tongue
WESTPHAL VARIANT has parkinsonism and not choreathetosis and is juvenile onset.
6. List the differential diagnosis for Parkinson's disease and Huntington's chorea.
Parkinson's Disease Differential
Parkinsonisum Plus Syndromes
-Don't respond to L-DOPA
1)Progressive Supranuclear Palsy
-early falls
-progerssive paralysis of voluntary eye movements. development of downgaze paresis
-oculovestibular responses stay intact
-Hummingbird sign in MRI
2)Multiple System Atrophy
a. Striatonigral Degeneration-Pyramidal Dysfunction
b. Olivopontocerebellar atrophy-Cerebellar Dysfunction
c. Shy Drager syndrome-Autonomic Dysfunction (including sever orthostatic hypotension)
3)Corticobasal degeneration
-Asymmetric motor findings
-Terrible Limb Apraxia
-Alien limb (autonomous behavior of a hand or arm)
Drug induced
-Neuroleptics (common)
-Metoclopromide (common)
-alpha-methyldopa
-reserpine
-Amiodarone
Toxic
-Cyanide
-Carbon Monoxide(bilateral pallidal necrosis on imaging)
-Manganese intoxication (seen commonly with liver cirrohsis, seen in welders, bright signal in basal ganglia on T1 MRI)
Wilson's Dz
-Copper metabolism screwed up
-Kayser-Fleischer Rings
-serum ceruloplasmin down urinary copper up
-liver disease
Focal Lesions
-vascular,neoplastic, and infectious lesions that can be detected on imaging)
Huntington's DZ Differential
Sydenham's Chorea
1) Post streptococcal
2) seen in conjunction with rheumatic fecer
3) ASO positive
4)self-limited
Chorea Gravidarum (Birth control Chorea)
-Caused by estrogen, with prior sydenham's chorea as a risk factor
Hyperthyroidism
Tardive Dyskinesia
-Prior neuroleptic use
-This is a real question b/c many have prior psych dz and have taken neuroleptics, which can be confused with Huntingtons
-Tardive Dyskinesia patients can hold their tongue in protrusion whil Huntingtons patients cannot
Wilson's Dz
-See parkinsons differential
Senile Chorea
-onset >60y/o
-No neuropsychiatric symptoms
Drugs
-Birth control
-L-dopa and other Dopamine agonists
-Stimulants
-Phenytoin
-Carbamazepine
-Ethosuximide
LECTURE 3
1.) Differentiate between the types of stroke(ischemic and hemorrhagic) and recognize transient iscemic attacks.
Ischemic Strokes
Ischemic strokes account for a majority of all strokes (75-85%).
There are two mechanisms:
1.) Vessels are occluded by buildup of arterial atherosclerotic plaques.
2.) Vessels are occluded by an embolus from another vessel.
Hemorrhagic Strokes
These occur when a blood vessel ruptures. These are associated with a high rate of morbidity and mortality.
There are two main types:
1.) Intracranial Hemorrhage (ICH)
2.) Subarachnoid Hemorrhage (SAH)
Common Causes:
1.) Hypertension-> ICH
2.) Aneurysmal Hemorrhage -> SAH (ciggarettes are a weak link)
3.) Subdural Hematoma
4.) AV Malformation
5.) Amyloid angiopathy
Transient Ischemic Attack
A brief episode of neurologic dysfunction from focal brainischemia or retinal ischemia with clinical symptoms lasting less than 1 hour without evidence of acute ifarct. After TIA there is a 10X risk of ischemic stroke. Peak risk is <= 3months with 50% chance within the first 48 hours. 2.) Given a clinical presentation recognize MCA, ACA, ICA strokes.
MCA: large portions of the frontal, parietal and temporal lobe
-Contralateral Hemiplegia
-hemianesthesia
-homonymous hemianopia
-When on dominant hemisphere you see aphasia when in non-dominant you see apraxia and/or sensory neglect
ICA: centrolateral portion of the cerebral hemisphere
Symptoms are identical to MCA except for occasional ipsilateral ocular symptoms (monocular blindness)
ACA: supplis medial portions of frontal and parietal lobes, corpus callosum, and ocasionaly caudate and internal capsule
-contralaterl hemiplegia (especially in the legs)
-grasp refelx
-urinary incontinence
Hints from class
if you see face and Arm you think MCA.
if you see leg you think ACA
if you see face arm and leg you think lacunar infarct
3.)Given a clinical presentation, recognize large vessel, lacunar, and embolic strokes.
Large Vessel Disease
This is the most common form of ischemic stroke. Subintimal plaques form @ or near bifurcations of arteries.
Mechanisms of ischemia:
1.) Flow Reduction
- High grade stenosis or occlusion
- usually distal to the bifurcation of the common carotid
- >70% stenosis is needed
2.) Artery to artery Embolism
- Non stenotic plaques <70%>Small Vessel Disease(lacunar)
These occur in penetrating arteries which originate from medium size vessels. Oclussion of the vessel causes a lacunar infarct (<1.5cm>Cardiogenic Embolism
Heartconditions which can lead to cardiogenic embolism
1.) non-rhematic AFIB (give warfarin to reduce stroke risk)
2.) acute MI
3.) prosthetic heart valves
4.) Other - rheumatic heart disease, Left ventricular throbi in previous MI, dilated cardiomyopathy, ventricular aneurysm, infective endocarditis and cardiac tumors.
Features for Clinical Diagnosis
1.) abrupt onset
2.) with cortical neurolgical deficit
3.) with potential source source of cardiac embolism
4.) Given a patient with a stroke, describte the diagnositc studies done for further evaluation.
1.) Blood Work
Everyone should get BGC, Serum Electrolytes, Renal Function Tests, CBC with plts, PT/INR and APTT. This is particularly important in assesing the possibility of using thrombolytics on the patient.
2.) Cardiac studies including EKG and echo
3.) CT/CTA
can be used to evaluate patients with symptoms of stroke and diagnose as hemorrhagic or ischemic. CTA can be used to find the particular area of the insult.
4.) MR/MRA
Can detect edema or swelling in advance of tissue destruction. However these studies tpically take a while, and often exaggerate the degree of stenosis. They can be used in a similar manner as CT/CTA.
5.) Angiography(CTA/MRA)
Can be used to determine etiology and/or outline treatment plans for patients. TPA can often be administered at the time of angiography. The TPA window is <<3 style="color: rgb(255, 0, 0);">5.) list the therapies for treatment of ischemic stroke.
Antiplatlet
This is the mainstay of stroke prevention. It is proven to reduce stroke in people with previous TIA and Stroke. Drugs include Aspirin and clopidrogel.
Warfarin
This is only recommended for the treatment of patients with AFIB.
Carotid Endarterectomy
In SYMPTOMATIC patients with recent TIA or stroke with ipsilateral carotid stenosis of >=70% can substantially benefit from carotid endarterectomy.
In ASYMPTOMATIC patients with >=60% stenosis and local surgical risk <3% should be considered for carotid endarterectomy.
ACUTE stroke
Don't overzealously treat mid to moderate hypertension, because this may help progression of nerve damage. Aspirin 60-300mg <=48 reduces risk of recrrence. tPA should be given if the patient can tolerate it and if <3hrs after stroke onset.
Ischemic Strokes
Ischemic strokes account for a majority of all strokes (75-85%).
There are two mechanisms:
1.) Vessels are occluded by buildup of arterial atherosclerotic plaques.
2.) Vessels are occluded by an embolus from another vessel.
Hemorrhagic Strokes
These occur when a blood vessel ruptures. These are associated with a high rate of morbidity and mortality.
There are two main types:
1.) Intracranial Hemorrhage (ICH)
2.) Subarachnoid Hemorrhage (SAH)
Common Causes:
1.) Hypertension-> ICH
2.) Aneurysmal Hemorrhage -> SAH (ciggarettes are a weak link)
3.) Subdural Hematoma
4.) AV Malformation
5.) Amyloid angiopathy
Transient Ischemic Attack
A brief episode of neurologic dysfunction from focal brainischemia or retinal ischemia with clinical symptoms lasting less than 1 hour without evidence of acute ifarct. After TIA there is a 10X risk of ischemic stroke. Peak risk is <= 3months with 50% chance within the first 48 hours. 2.) Given a clinical presentation recognize MCA, ACA, ICA strokes.
MCA: large portions of the frontal, parietal and temporal lobe
-Contralateral Hemiplegia
-hemianesthesia
-homonymous hemianopia
-When on dominant hemisphere you see aphasia when in non-dominant you see apraxia and/or sensory neglect
ICA: centrolateral portion of the cerebral hemisphere
Symptoms are identical to MCA except for occasional ipsilateral ocular symptoms (monocular blindness)
ACA: supplis medial portions of frontal and parietal lobes, corpus callosum, and ocasionaly caudate and internal capsule
-contralaterl hemiplegia (especially in the legs)
-grasp refelx
-urinary incontinence
Hints from class
if you see face and Arm you think MCA.
if you see leg you think ACA
if you see face arm and leg you think lacunar infarct
3.)Given a clinical presentation, recognize large vessel, lacunar, and embolic strokes.
Large Vessel Disease
This is the most common form of ischemic stroke. Subintimal plaques form @ or near bifurcations of arteries.
Mechanisms of ischemia:
1.) Flow Reduction
- High grade stenosis or occlusion
- usually distal to the bifurcation of the common carotid
- >70% stenosis is needed
2.) Artery to artery Embolism
- Non stenotic plaques <70%>Small Vessel Disease(lacunar)
These occur in penetrating arteries which originate from medium size vessels. Oclussion of the vessel causes a lacunar infarct (<1.5cm>Cardiogenic Embolism
Heartconditions which can lead to cardiogenic embolism
1.) non-rhematic AFIB (give warfarin to reduce stroke risk)
2.) acute MI
3.) prosthetic heart valves
4.) Other - rheumatic heart disease, Left ventricular throbi in previous MI, dilated cardiomyopathy, ventricular aneurysm, infective endocarditis and cardiac tumors.
Features for Clinical Diagnosis
1.) abrupt onset
2.) with cortical neurolgical deficit
3.) with potential source source of cardiac embolism
4.) Given a patient with a stroke, describte the diagnositc studies done for further evaluation.
1.) Blood Work
Everyone should get BGC, Serum Electrolytes, Renal Function Tests, CBC with plts, PT/INR and APTT. This is particularly important in assesing the possibility of using thrombolytics on the patient.
2.) Cardiac studies including EKG and echo
3.) CT/CTA
can be used to evaluate patients with symptoms of stroke and diagnose as hemorrhagic or ischemic. CTA can be used to find the particular area of the insult.
4.) MR/MRA
Can detect edema or swelling in advance of tissue destruction. However these studies tpically take a while, and often exaggerate the degree of stenosis. They can be used in a similar manner as CT/CTA.
5.) Angiography(CTA/MRA)
Can be used to determine etiology and/or outline treatment plans for patients. TPA can often be administered at the time of angiography. The TPA window is <<3 style="color: rgb(255, 0, 0);">5.) list the therapies for treatment of ischemic stroke.
Antiplatlet
This is the mainstay of stroke prevention. It is proven to reduce stroke in people with previous TIA and Stroke. Drugs include Aspirin and clopidrogel.
Warfarin
This is only recommended for the treatment of patients with AFIB.
Carotid Endarterectomy
In SYMPTOMATIC patients with recent TIA or stroke with ipsilateral carotid stenosis of >=70% can substantially benefit from carotid endarterectomy.
In ASYMPTOMATIC patients with >=60% stenosis and local surgical risk <3% should be considered for carotid endarterectomy.
ACUTE stroke
Don't overzealously treat mid to moderate hypertension, because this may help progression of nerve damage. Aspirin 60-300mg <=48 reduces risk of recrrence. tPA should be given if the patient can tolerate it and if <3hrs after stroke onset.
Lecture 9 - Multiple Sclerosis and related disorders
1. Describe the natural history of multiple sclerosis in terms of
a. Percentages who progress to significant disability
Most patients will (see below). Only 5% have a benign clinical course.
b. Percentages who require ambulatory assistance after 10 years
50% will require a cane to ambulate, and 15% will require a wheelchair
c. Percentages who develop secondary progressive MS
50% within 10 years. 85-90% within 25 years.
2. Describe four characteristics that predict a severe course of MS.
Severe course
Males have a more severe course than females
Motor and cerebellar symptoms
Disability after the first attack
Short time interval between attacks
Numerous relapses within the first year
Burden of disease on MRI – >10 lesions on MRI at diagnosis indicates walking with a cane within 14 years
Change in lesion load within the first year
Less severe course
Sensory symptoms
Infrequent attacks,
Full neurological recovery after an attack
Low level of disability after 5-7 years
Burden of disease on MRI – No lesions on MRI at diagnosis indicates no significant disease within 14 years
3. Given the presentation of a patient with MS, characterize whether the patient has clinically isolated MS syndrome, relapsing remitting MS, secondarily progressive MS, or primary progressive MS.
Clinically isolated MS syndrome – one symptom or abnormality on clinical exam, w/o evidence of the classic adage “lesions in time and space” – a.k.a., there is clinical evidence of a single demyelinating lesion. May then progress to RRMS, especially if patient has additional clinically silent lesions on MRI.
Relapsing remitting MS – 85% – patients have relapses or exacerbations during the course of their disease comprised of symptoms such as visual blurring (optic neuritis), diplopia, vertigo, numbness, parasthesias, and weakness (myelopathy). Between attacks most patients have incomplete recovery, showing slight residual symptoms that lead to cumulative disability.
Secondarily progressive MS – 85% of RRMS, w/o treatment – characterized by more pronounced, steady, progressive decline in function +/– superimposed relapses. Most common symptoms are myelopathic ones – ambulation difficulties, bladder, bowel, and sexual dysfunction.
Primary progressive MS – 10-15% - gradual decline from the onset, typically with myelopathic features.
Progressive relapsing MS – 1% total – a subset of PPMS w/ rare relapses superimposed upon a slow progression.
Differentiating relapse from symptom exacerbation…
Relapse – due to production of a new lesion, or reactivation of an old lesion
Increase in size of lesion on MRI
Renewed gadolinium enhancement on MRI
Symptoms are persistent >1-2 days
Exacerbation – an old, quiescent lesion gets worse – due to heat, fatigue, infection (UTI, URI)
Symptoms may fluctuate over the course of the day
New gadolinium enhancement on MRI
Symptoms should resolve w/I 1-2 days of the inciting factor removal/treatment
4. Given a clinical presentation and an MRI of the head, be able to diagnose MS.
Clinical presentation – Need evidence of “multiple lesions in time and space”
Optic neuritis
Transverse myelitis
Intranuclear ophthalmoplegia
Spasticity
Fatigue
Urinary sphincter dysfunction
Incoordination
Nystagmus
NOT seizures (he says this is almost exclusionary for the dx) or cognitive decline
Spinal tap – positive oligoclonal bands and elevated IgG index and synthesis rate
May see mild lymphocytic pleiocytosis
MRI findings
Dawson’s fingers: Periventricular, perpendicular, ovoid lesions either in the cerebral hemispheres or infratentorially. Best seen on flair images (dark CSF).
Cervical cord lesions – cigar-shaped, typically span 1-2 segments, predilection for cervical cord. Best seen on proton density and T2 images (bright CSF).
Deep white matter and juxtacortical lesions (not specific)
Lesions often enhance with gadolinium contrast – distinguishes active inflammation from chronic lesions.
5. Given a patient presenting with signs and symptoms of MS, recognize Lhermittes sign, intranuclear ophthalmoplegia, optic neuritis, and transverse myelitis.
Lhermittes sign – sensation of “electrical shock” down the spinal column provoked by neck flexion
Intranuclear ophthalmoplegia
· Intact abduction with slowed or absent adduction of contralateral eye
· Often bilateral
· Due to destruction of the medial longitudinal fasciculus
Optic neuritis – inflammation and demyelination of the optic nerve
· Unilateral loss of acuity or color detection, occasionally blindness
· Concomitant pain w/ ocular movement
· Central or centrocecal defect (can’t see center part of visual field), a quadrantoanopia, a horizontal altitudinal defect, or enlargement of the blind spot
· Marcus Gunn pupil – afferent papillary defect – pupil constricts less (appears to dilate) in response to light
· Optic disc may have anterior swelling and edema leading to pallor over time
Transverse myelitis
· Predilection for posterior columns
· Loss of vibratory and proprioceptive senses
· Sensory ataxia
· Lower extremity spasticity
· Sphincter and sexual dysfunction
· May be related to Lhermitte’s sign
-CV
Any comments, corrections, or addendums, leave them below. :)
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