Random Facts Flashcards
(169 cards)
1
Q
What is a supranuclear gaze palsy and its symtpoms?
A
Lesion in a cortical gaze center and only voluntary gaze is impaired. Reflexes still intact
2
Q
What is a nuclear gaze palsy and its symptoms?
A
lesion in a brainstem gaze center and there is no voluntary or reflexive conjugate eye movement
3
Q
What is internuclear ophthalmoplegia?
A
lesion in MLF whcih connects the CN6 nucleus and CN3 nucleus on contralateral sides, inhibiting conjugate eye movement.
4
Q
What are the symptoms of INO if R. MLF lesion?
A
Cannot adduct right eye (R. medial rectus not innervated). Will see a nystagmus in the left eye.
5
Q
Are dysarthria and dysphagia sxs of LMN or UMN lesion?
A
LMN. Will not see sxs if there is a unilateral UMN lesion because the nucleus ambiguus has bilateral cortical input. (CNIX and CNX)
6
Q
What are the sxs of peripheral nerve lesion to CNXI?
A
- ipsilateral weakness of shoulder shrug (ipsilateral trapezius weakness)
- weakness when turning the head to the side opposite the lesion (ipsilateral SCM weakness)
7
Q
What are the sxs of unilateral central nerve lesion to CNXI?
A
- Weak shrug of contralateral shoulder (contralateral trapezius affected)
- Weak turning of head to ipsilateral side (ipsilateral SCM affected)
8
Q
Sxs of lesion to unilateral peripheral CNXII?
A
Weakness of ipsilateral tongue muscles. Cannot protrude tongue to the opposite side.
9
Q
What parts of the body does the common peroneal nerve innervate?
A
Lateral leg and the dorsum of the foot
10
Q
What part of the body does the tibial nerve innervate?
A
sole of the foot
11
Q
If someone cannot perform the rhomberg test successfully, is it a positive or negative test?
A
Positive rhomberg test
12
Q
What is baclofen and what does it treat?
A
GABA receptor agonist that is used to treat spacticity. May be used for dystonias.
13
Q
What is the best treatment for dystonias?
A
high frequency stimulation of the globus pallidus pars interna (GPi) through surgical placement of a deep brain stimulator
14
Q
What parts of the brain show abnormal activity in dystonia?
A
low/abnormal activity of the basal ganglia output structures including the internal part of globus pallidus and substantia nigra pars interna.
15
Q
what is the most common cause of early onset generalized dystonia?
A
DYT-1
16
Q
What are the structural/genetic abnormalities found in DYT-1?
A
GAG deletion in exon 5 of DYT-1 (TOR1A)
17
Q
What drug may prove useful in treating dystonia?
A
trihexyphenidyl (antimuscarinic) used to treat parkinson’s
18
Q
Is DYT-1 usually associated wtih sensory findings?
A
No!
19
Q
What is the most common cause of tardive dyskinesia?
A
chronic exposure to central dopamine blocking agents like neuroleptics (ex: metoclopramide for gastroparesis, typical antipsychotics)
20
Q
What are the stongest risk factors for tardive dyskinesia?
A
Old age, female gender, and coexistent brain damage.
21
Q
Common symptoms of tardive dyskinesia?
A
arching spasms of the back and neck.
22
Q
What is the treatment for tardive dyskinesia?
A
benzos, baclofen, Vitamin E
23
Q
MOA of reserpine and tetrabenazine?
A
they do not deplete dopamine and therefore do not cause tardive dyskinesia
24
Q
What nerve is likely to be injured in an anterior dislocation of the humeral head?
A
axillary nerve
25
Describe the tremor characteristic of Parkinson's Disease
**Resting tremor**: (4-6Hz) and decreases with voluntary movement. In the legs and hands, facial involvement less common
26
Describe an essential tremor?
Bilateral tremor of the hands (usually no legs) but can involve some head tremor without dystonia. No other neurological signs are usually present and tremor can be **relieved by alcohol**
27
Describe a cerebellar tremor?
ataxia, dysmetria and gait d/o present. tremor increases steadily as the hand reaches its target.
28
Describe a physiologic tremor
low amp (10-12Hz so not visible under normal conditions). there is acute onset with increased sympathetic activity (drugs, caffeine, anxiety, hyperthyroidism). Usually worse with movement and can involve the face and extremities.
29
What is fetal hydantoin syndrome?
Usually occurs when mother is on phenytoin or carbamazepine during pregnancy. Baby will present at birth with small body size, microcephaly, cleft lip and palate, digital hypoplasia, hirsutism and developmental delay.
30
What characteristics are used to describe 'flaccid'?
LMN weakness with hypo- or areflexia, hypotonia, and muscle atrophy if there is chronic disease
31
What is the primary concern in GBS?
First priority should be to determine th eprogression of respiratory insufficiency by serially measuring FVC. If FVC gets below 15-20 mL/kg, then elective intubation should be performed.
32
What type of paralysis is seen in GBS?
**Acute flaccid paralysis**. Starts distally and ascends. Can eventually affect cranial nerves and diaphragm. Can progress over hours to days.
33
What are the 5 types of Guillian-Barre Syndrome?
1. AIDP
2. Miller-Fischer variant
3. Acute motor-axonal neuropathy (AMAN)
4. Acute motor-sensory axonal neuropathy (AMSAN)
5. Acute panautonomic neuropathy
34
What are the characteristics of Miller-Fischer varient?
triad of areflexia, ataxia (out of proportion to sensory defects) and ophthalmoplegia. Mainly cranial nerve weakness rather than extremities and a positive anti-GQ1b (ganglioside) antibodies.
35
What are the characteristics of AMAN (acute motor-axonal neuropathy)?
purely motor; affects mainly children and 70% is due to C. jejuni
36
What are the characteristics of AMSAN (motor-sensory)?
maily affects adults with significant muscle atrophy and poor recovery.
37
What should be on the differential diagnosis for an acute flaccid paralysis?
1. GBS
2. botulism (dozen Ds)
3. tick paralysis
38
What is the primary lab finding seen in GBS?
Should perform a lumbar puncture which will show rising protein levels up to 400mg/L with no associated increase in cell count (**albuminocytologic dissociation**)
39
What treatments have been proven useful in GBS?
Plasmaphoresis \> IVIg. Steroids DO NOT work.
40
What is Holmes-Adie syndrome?
typically seen in young women and associated with unilateral unresponsive pupil and depressed deep tendon reflexes in the legs
41
How do you differentiate a tonic pupil from a third nerve palsy?
Check for pupillary response on accomodation. Constriction of the pupil on accomodation is seen with Holmes-adie syndrome, but not seen in third nerve palsy. (both third nerve palsy and holmes-adie will be unresponsive to light)
42
How is the diagnosis of Holmes-Adie syndrome confirmed?
Add 0.1% pilocarpine to the affected eye. If it constricts, then diagnosis of Holmes-Adie is confirmed.
43
Which pupillary muscles are controlled by sympathetics and by parasympathetics?
Sympathetics - dilator muscle (mydriasis)
Parasympathetics - sphincter muscle (miosis)
44
Where are the cell bodies for parasympathetic nerves involved in pupillary movement located?
parasymp preganglionic= edinger-westphasl nucleus of upper midbrain
parasymp postganglionic= ciliary ganglion
45
Where are the nerve cell bodies for sympathetic pupillary movment located?
sym preganglionic= Budge-Waller (intermediolateral gray matter of cord segments C8-T2). Ascend in sympathetic chain then synapse at superior cervical ganglion.
sym postganglionic= travel superficially on ICA until cavernous sinus when the nerve joints the ophthalmic division of trigeminal nerve and enters the orbit with nasociliary nerve to innerate dilator muscle via long ciliary nerves.
46
What is a tonic pupil?
Pupil that lost its parasympathetic innervation, therefore looks bigger than other pupil and does not constrict to light. However, can slowly accomodate.
47
What causes tonic pupil?
dysfunction of the ciliary ganglion or the short ciliary nerves
48
What is an argyll-roberstonian pupil?
Seen in neurosyphilis. Pupils will be miotic, unresponsive to light but able to accomodate (similar to adie pupils however adie are bigger at rest)
49
What is the treatment for Holmes-Adie syndrome?
Reasurrance that it is a benign condition. Can treat the blurry vision with contact lens with an artificial pupil.
50
What is a TIA (transient ischemic attack)?
cerebral ischemic event with focal neurologic deficits lasting less than 24 hours (usually several minutes to 1-2 hours. DWI can show if there was an infarct after the symptoms resolve)
51
What is Todd's Paraylsis?
brief period of temporary paralysis following a seizure
52
If a stroke is suspected, what type of a workup must be ordered?
CT w/o contrast. Later when the patient is stable can get an MRI. Need to get an EKG, CBC, glucose, PT and PTT. Can also get a carotid ultrasound (duplex), transcranial Doppler, echocardiogram, magnetic resonance angiogram (MRA) of head and neck, and/or cerebral angiogram (CA).
53
If someone has a hemorrhagic stroke, do you still treat with a blood thinner to prevent DVT?
YES! All patients with ischemic of hemorrhagic stroke must receive DVT prophylaxis.
54
What are the major risk factors for stroke?
Same as coronary heart disease (age, hypertension, smoking, diabetes, hyperlipidemia, heart disease and family history).
55
What are the most common causes of ischemic stroke?
Cardiac embolism, large-vessel atherothrombosis, and small vessel intracranial occlusive disease
56
What are the common sources of cardiac embolism?
afib, mechanical prosthetic heart valves, acute MI, and low left ventricular ejection franction, focal mocardial hypokinesis, patent foramen ovale and endocarditis
57
What are the common effects of large bessel atherosclerosis?
Affects the carotid bifurvation, major intracranial vessels, or the extracranial vertebral artery.
58
What characterizes small vessel strokes (aka lacunar strokes)?
Usually are pure motor, pure sensory, ataxic hemiparesis, dysarthria/clumsy hand. Usually related to hypertension and/or diabetes
59
If a patient has a history of afib, is long term treatment with anticoagulation or antiplatelet drugs preferred?
anticoagulation (warfarin).
60
What are the risk factors for subarachnoid hemorrhage?
age (50yo), gender (f\>m), hypertension and tobacco use
61
When is post aneurysmal subarachnoid hemorrhage most likely to occur?
4-14 days after the initial insult. Detect via transcranial doppler.
62
What is the most sensitive neuroimaging study for detecting SAH bleed?
Head CT w/o contrast. Most sensitive 24 hours after bleed.
63
If head CT is negative, what is performed next in suspected SAH?
LP performed, will show **xanthochromia** (yellow CSF) if positive for SAH. Most sensitive 12 hours post onset.
64
What is the mortality rate of SAH within the first 30 days?
60% die in the first 30 days, 10% die instantly.
65
What is the treatment in low grade acses of SAH?
Coiling has been shown to be superior to clipping in low grade SAH.
66
What is the treatment of high grade SAH?
Clipping should be performed in the first 48 hours or delayed for 2 weeks to avoid the window of greatest risk for vasospasm.
67
What treatment is preferred to prevent vasospasm?
Triple H therapy (hypertensive hypervolemic hemodilution) to maintian cerebral perfusion pressure and nimodipine a CCB.
68
What are the most common causes of SAH?
ruptured saccular or berry aneurysms azccount for 80% of nontrauamtic SAH and have the worst prognosis.
69
What are common findings in SAH?
hyponatremia due to elevated ANP (can cause seizures), ECG changes like QT prolongation, T-wave inversion and arrhythmias
70
What is the most sensitive study for vasospasm?
transcranial doppler study
71
What is a cryptogenic stroke?
Stroke that occurs in patients less than 55yo
72
What is seen on neuroimaging studies of patients with schizophrenia?
loss of cortical tissue volume with **enlarging lateral ventricles**
73
What is seen on neuroimaging for autism, panic d/o, OCD, and PTSD?
Autism- increased total brain volume
OCD- abnormalities in orbitofrontal cortex and striatum
Panic d/o- decreased volume of amygdala
PTSD- decreased hippocampal volume
74
What is seen in the brain after diffuse axonal injury?
numerous punctuate hemorrhages with blurring of the gray-white matter interface.
75
What is the classic triad of a brain abscess?
1. Fever
2. Severe headaches (nocturnal or morning)
3. Focal neurological changes
(seizures are the presenting sxs of brain abscesses in 25% of cases)
76
What are the characteristics of a complex partial seizure?
Last for a few minutes, impaired consciousness, staring spells, automatisms (lip smacking, hand movements), and post-ictal confusion. EEG normal. Hyperventilation has no effect.
77
What is juvenile myoclonic epilepsy?
myoclonic seizures that occur shortly after awakening and generalized tonic-clonic seizures that are triggered by sleep deprivation. Responds well to valproic acid treatment
78
What should be on the differential if there is T wave inversion?
MI, myocarditis, old pericarditis, myocardial contusion and digoxin toxicity.
79
What does the brain look like in Sturge-Weber d/o?
intracranial calcifications that resemble a tram line
80
What is first line treatment for migraines in children less than 12yo?
Supportive management and administration of acetominophen or an NSAID
81
What is the only CN symptom of pseudotumor cerebri?
6th nerve palsy
82
How does acetazolamide help in treating idiopathic intracranial hypertension (IIH aka pseudotumor cerebri)?
inhibits choroid plexus carbonic anhydrase therefore decreasing the production of CSF.
83
What drug treats tremor in Parkinson's Disease?
trihexyphenidyl- anticholinergic
84
What is the first line treatment of narcolepsy?
modafinil- stimulant
85
What is the function of pramipexole?
treats the sxs of Parkinson's disease and Restless Leg Syndrome
86
What d/o does head trauma cause which in turn causes delium or altered mental status?
SIADH which can cause hyponatremia and delirium
87
What are the most common medications used to treat delirium?
lorazepam, haloperidol or risperidone.
88
How is delirium diagnosed?
Clinical diagnosis. Can be supported with lab evals such as CMP, CBC, glucose, BUN, liver function studies, electrolyte levels, thyroid function studies and ammonia (hepatic encephalopathy)
89
How long does delirium usually last?
Usually lasts approximately 1 week, although it can take several weeks for cognitive function to return to normal levels. Full recovery is common.
90
Is infant botulinum an ascending or descending paralysis?
descending paralysis
91
What is bilateral bulbar palsy and what d/o is it associated with?
ptosis, sluggish pupillary response to light, poor suck and gag reflex. Seen in infant botulinum.
92
What is diagnostic of a craniopharyngioma?
presence of a cystic calcified parasellar lesion on MRI. Will most likely also see increased intracranial pressure
93
What are the common sxs of increased intracranial pressure?
headache, vomiting
94
What are the signs and sxs of spinal cord compression?
UMN dysfunction distal to the site of compression. Weakness, hyperreflexia and extensor plantar response
95
What is the treatment of acute exacerbations of MS?
IV corticosteroids
96
Is tick-borne paralysis ascending or descending?
ascending
97
What are the sxs of tick-borne paralysis?
rapidly progressive (hours) ascending paralysis, absense of fever, absence of sensory abnormalities, and normal CSF examination.
98
How does CO2 affect intracranial pressure?
Decreased CO2 levels leads to decreased intracranial pressure via **vasoconstriction**
99
How can you differentiate between primary CNS lymphoma and cerebral toxoplasmosis?
**Primary CNS lymphoma**- weakly ring-enhancing solitary lesion in the periventriclar area with the presence of EBV DNA in the CSF.
**Toxoplasmosis**- multiple ring-enhacing lesions in the basal ganglia
100
What is the finding in a brain that has undergone status epilepticus?
**Cortical laminar necrosis**. Due to prolonged seizures and cytotoxicity.
101
What are the sxs of CJD?
Rapidly progressive dementia (few weeks) seen in patients aged 50-70yo. May have myclonus, akinetic mutism, cerebellar or visual distrubances, hypokinesia, periodic sharp wave complexes on EEG, or positive 14-3-3 CSF assay.
102
What is the most common cause of vertigo?
Benign Paroxysmal Positional Vertigo (BPPV)
103
What is the preferred abortive treatment of cluster headaches?
nasal 100% oxygen
104
What is posterior vermis syndrome?
truncal dystaxia. Unbalanced gait, horizontal nystagmus, and papilledema
105
What typie of hematoma is characterized by a lucent period?
EDH
106
Where is an EDH most likely to occur?
in the temporoparietal area and resulrt from a tear of the middle meningeal artery
107
What is cushing response?
caused by increasing ICP and results in **hypertension, bradycardia, and bradypnea**
108
What diagnostic studies should be ordered in EDH?
CBC, PT/aPTT, fibrin split products, serum chemistries, toxicology screen,
109
What is a concussion?
brief, transietnt loss of consciousness assocaiated with a short period of amnesia caused by blunt head trauma or sudden develeration
110
What is postconcussion syndrome?
4 weeks after the initial concussion, patients can develop more extensive sxs such as irritibility, depression, insomnia and subjective intellectual dysfunction
111
WHy do patients with PCS experience memory impairment?
due to inability/difficulty concentrating
112
Do simple partial or complex partial seizures have LOC?
complex partial seizures
113
What is the most common aura for a focal onset seizure?
abdominal discomfort
114
Where do complex partial seizures usually arise?
temporal lobe
115
What type of seizure is associated with automatisms?
complex partial seizures (NOT absence)
116
What are atypical absence seizrues?
if the beginning and end of the absence spell is not distinct, or if tonic and autonomic componenets also occur
117
What type of seizure is associated with cysticercosis?
complex partial seizures
118
Can lacunar infarcts be seen on CT?
no, they are usually thrombotic in nature but are really small so they cannot be seen on CT
119
What is the most common site for a lacunar stroke?
posterior limb of the internal capsule. Will get a pure motor stroke.
120
What type of a seizure is more likely to accompany bowel and bladder loss of control?
partial seizures that become secondarily generalized
121
What are the presenting sxs of central cord syndrome?
weakness that is more pronounced in the upper extremities. Might also have damage to pain and temp in the upper extremities if the ALS is affected.
122
What type of injury most commonly causes central cord syndrome?
hyperextension injuries and pre-existing degenerative changes in the cervical spine.
123
What are the presenting sxs of anterior cord syndrome and what causes it?
Presents with bilateral spastic motor paresis distal to the lesion and is due to occlusion of the anterior spinal artery.
124
What is neuropathic claudication? What d/o is it usually used to describe?
Neuropathic claudication is used to talk about the exacerbation of lumbar stenosis leg symptoms when walking.
125
What is amaurosis faux?
painless loss of vision due to emboli. Must get a carotid duplex done to check for embolis. This is a warning sign of an impending stroke.
126
What does "brain dead" entail?
Absent cortical and brainstem functions. Spinal cord may still be functioning, so might still be able to see deep tendon reflexes.
127
What are the long-term neurologic sequelae associated with bacterial meningitis?
Hearing loss, loss of cognitive functions (due to neuronal loss in the dentate gyrus of the hippocampus), seizures, mental retardation, and spasticity or paresis
128
What is subacute combined degeneration?
Due to vitamin B12 deficiency. Causes a progressive symmetric polyneuropathy greater in the legs than in the arms. First affects dorsal column, and later can affect corticospinal tracts causing UMN signs.
129
What are the sxs of acute angle-closure glaucoma?
Usually occurs in women and presents with rapid onset severe eye pain and seeing halos of light. Affected pupil will be dilated and poorly responsive to light. Patients develop tearing and headache w/N&V as IOP increases. Can lead to permanent vision loss
130
What medications can cause acute angle-closure glaucoma?
anticholinergics (tolterodine), sympathomimetics, and decongestants
131
Does cauda equina syndrome cause upper or lower motor neuron signs?
lower motor neuron- since the nerve roots are affected and they are a part of the peripheral nervous system
132
Does conus medullaris syndrome cause upper or lower motor neuron signs?
upper and lower motor neuron signs since the conus is a part of the spinal cord
133
What are the steps in management of CES (cauda equina syndrome)?
emergency MRI, neurosurgical eval, and IV glucocorticoids
134
What is the treatment of simple and complex febrile seizures?
**Simple**- reassure the parents that the child is okay and can be taken home. Provide adequate hydration.
**Complex**- abortive therapy if the seizure lasts longer than 5 minutes (rectal benzos)
135
What is the most significant complication of pseudotumor cerebri?
blindness
136
What is the pathophysiology of pseudotumor cerebri?
there is impaired absorption of the CSF by the arachnoid villi causing the increased ICP, papillidema, headache, etc
137
What are the sxs of infectious cavernous sinus thrombosis?
sxs are due to increasing ICP and include headache, papilledema, vomiting, periorbital edema, binocular palsies, hypoesthesia and hyperesthesias. THese symptoms can rapidly become bilateral due to the anastomosis in the cavernous sinus between both sides. (CN 3, 4, 5, 6 sxs)
138
What is infectious cavernous sinus thrombosis?
When there is a facial infection, it can travel through the valveless ophthalamic/facial venous system and enter the cavernous sinus and cause thrombosis or increased intracranial pressure.
139
How do you diagnose and treat cavernous sinus thrombosis?
MRI with MR venography and treat with IV antibiotics
140
What is the pathophysiology of myasthenia gravis?
autoantibody to the acetylcholine receptor. Only motor nerves are affected, so no sensory deficits. Don't forget to check for a thymoma on chest CT!
141
What is the most common site of hypertensive hemorrhages?
30% of hypertensive hemorrhages occur in the putamen and almost always involves the adjacent internal capsule thus resulting in contralateral dense hemiparesis. (usually the same location as lacunar hemorrhages are found- putamen\>thalamus\>pons\>cerebellum\>cortex)
142
What is pseudodementia? How does it differ from Alzheimers?
severe depression in older adults that presents with features similar to dementia. They have difficulty with attention, concentration, and memory. Different from Alzheimers because people with pseudodementia are often frightened by their lack of memory.
143
How should pseudodementia be treated?
SSRIs
144
What is the first and second most common CNS tumor in children?
1. Benign astrocytoma
2. Medulloblastoma (posterior fossa)
145
What is the inheritence pattern and treatment of essential tremor?
autosomal dominant
propanolol
146
What is the treatment of myasthenia crisis?
Plasmaphoresis OR IVIg and glucocorticoids. Intubation if necessary.
147
What is the most common type of seizure in adults with epilepsy?
complex partial seizures
148
What is catamenial seizure exacerbation or catamenial epilepsy?
Woman will have doubled seizure frequency when they have their period.
149
What is sick sinus syndrome?
type of bradycardia in which the SA or sinus node is not working correctly. Most commonly due to normal aging, but can also result from tachyarrhythmias due to Wolff-Parkinson-White syndrome or prolonged-QT interval
150
What is the definitive treatment of sick sinus syndrome?
permanent pacing to avoid an onset of fatal arrhythmia or sinus arrest
151
What are the sxs of sick sinus syndrome?
Rapid LOC without warning and with abrupt halt in episode and no postevent discomfort. Sxs are not positional
152
What are the sxs of a pseudoseizure?
Patients **bilaterally** seizure but maintain normal consciousness, no urinary incontinence or tongue biting. Normal EEG monitoring during an event.
153
What is Biswanger disease?
cerebrovascular disease especially as a result of long-standing hypertension, can debelop diffuse subcortical white matter changes seen on imaging and an insidious rather than sudden stepwise decline in cognitive function
154
What are the three treatments currently available for Alzheimer's Disease?
donepezil, rivastigmine, and galantamine. Memantine has also been proven to help in later stages of dementia.
donepezil (aricept) and rivastigmine (exelon) are cholinesterase inhibitors
memantine (NMDA receptor antagonist)
155
What is characteristic behavior associated wtih DLBD is seen on PET scan?
decreased occipital lobe blood flow or metabolism
156
How is acetylcholine metabolism compare between DLBD and AD?
DLBD has greater loss of acetylcholine and a smaller loss of ACh-receptors
157
What classifies Parkinson Disease dementia?
This is when the parkinsonism preceds cognitive dysfunction by more than 2 years. (DLBD is when dementia precedes motor signs. Dementia is associated with bisual hallucinations and episodes of reduced responsiveness)
158
What is the pathology of DLBD?
alpha-synuclein found in Lewy Body inclusions (alpha-synuclein also seen in PD and AD)
159
What are the 3 most common dementias?
1. Alzheimers
2. Vascular dementia
3. Diffuse lewy body dementia (DLBD)
160
What dementia is associated with REM-related behavior disorders as one of the presenting symtpoms?
Diffuse Lewy Body dementia
161
What is seen on imaging in B12 deficiency subacute combined degeneration of the spinal cord?
increased signal intensity on T2-weighted images, primarily in the dorsal columns and lateral pyramidal tracts
162
How can you differentiate between MS and Subacute combined degeneration of the spinal cord?
MS is mainly CNS d/o and does NOT affect peripheral nerve conduction. Slowed nerve conduction is seen with B12 deficiency
163
What is the treatment of optic neuritis?
IV methylprednisolone
164
What two drugs can cause optic neuritis?
amiodarone and ethambutol
165
What is Acute Disseminated Encephalomyelitis (ADEM)?
acute, uniphasic syndrome, caused by immune-mediated inflammatory demyleination, often postviral illness (1-3 weeks post) or after vaccinations. Associated with headache, confusion, and spinal cord compromise. Hard to differentiate from MS.
166
What is acute necrotizing hemorrhagic encephalomyelitis (ANHE)?
hyperacute form of ADEM; similar symptoms and cause
167
What is the primary histological finding in AEDM?
perivenular demyelination with relative sparing of axons. Lesions more commonly in the **thalamus** (absence of oligoclonal bands in CSF; helps differentiate from MS)
168
If a patient presents with sxs of meningitis and has a macular papular rash, what should be done next?
Suspected meningococcal meninigitis. Treat with IV penicillin G or ampicillin and obtain labwork asap
169
What is the most common site for entrapment of the ulnar nerve?
the elbow
