Ch. 15 Neuro Flashcards
1
Q
What percent of strokes are ischemic vs hemorrhagic?
A
85% ischemic
15% hemorrhagic
2
Q
What is the most common cause of stroke in the US?
A
thrombotic – results from clot formation at the site of an ulcerated atherosclerotic plaque
3
Q
What are the two types of thrombotic strokes?
A
Lacunar - stroke of a small terminal vessel
Cortical
4
Q
How is Cerebral Perfusion Pressure calculated?
A
CPP = MAP - ICP
5
Q
What is the NIH Stroke Scale range?
A
0 to 42
6
Q
What is amaurosis fugax?
A
transient monocular blindness from embolization of carotid plaque to the ophthalmic artery
7
Q
How is TIA defined?
A
transient neurologic deficits lasting < 1 hour with no evidence of infarction on brain
imaging studies (MRI)
8
Q
What is Wernicke aphasia?
A
receptive aphasia – an inability to comprehend language input; speech is fluent but disorganized
9
Q
Where is Wernicke’s ares?
A
Temporal lobe
10
Q
What is Broca aphasia?
A
expressive aphasia – inability to communicate verbally. Speech is halting and
produced with great effort
11
Q
Where is Broca area?
A
frontal lobe
12
Q
The hallmark of ________ circulation
stroke is crossed deficits (eg, sensory loss
on right side of face vs left side of body).
A
posterior
13
Q
In hypertensive patient, where you are trying to lower BP to give TPA, which two medications are first line?
A
Labetalol, Nicardipine
14
Q
What artery is implicated with:
Contralateral weakness of leg > arm and face with minimal sensory findings
A
Anterior cerebral artery
15
Q
What artery is implicated with:
Contralateral weakness AND numbness of arm and face > leg
A
Middle cerebral artery (most common)
16
Q
In a middle cerebral artery stroke you may see a gaze preference for which side?
A
Gaze preference toward size of infarct
17
Q
What artery is implicated in clumsy hand–dysarthria syndrome?
A
Lacunar artery?
18
Q
What artery is implicated if:
Contralateral visual field and light touch/pinprick deficit with minimal weakness
A
Posterior Cerebral Artery
19
Q
What artery is implicated if:
Crossed deficits: ipsilateral cranial nerve deficits with contralateral weakness
A
Vertebrobasilar artery
20
Q
What artery is implicated in “Locked in” syndrome?
(complete paralysis of voluntary muscles except eye movement; normal level of consciousness)
A
Basilar artery
21
Q
What artery is implicated:
Sudden inability to walk or stand with
headache, vertigo, nausea/vomiting,
abnormal gait, CN abnormalities
A
Cerebellar artery
22
Q
What glucose level is a contraindication to tPA?
A
> 400
23
Q
What is the dose for tPA for stroke?
A
0.9 mg/kg with 10% given as bolus, remaining infused over 60 minutes.
Ex: 80 kg person: 72 mg total; 7.2 mg bolus, 64.8 mg infusion over remaining hour
24
Q
If symptomatic intracranial hemorrhage (SICH) is confirmed with non-contrast CT, which thrombolytic and anti-platelet reversal agents should be considered?
A
FFP, platelets, cryoprecipitate
25
Aspirin should be given within ___ hours (unless thrombolysis candidate) for secondary stroke prevention.
48 hours
26
In secondary stroke prevention, what medications should be given if ASA allergy?
Clopidogrel (or ticlopidine)
27
Is routine seizure prophylaxis recommended in CVAs?
NO
28
What role does heparin have in CVAs?
No proven benefit in acute stroke
29
What is the ABCD^2 score used for?
predict likelihood of subsequent stroke within 2 days
30
What variables are included in ABCD^2 score to predict subsequent stroke in patients with TIA?
age >60y
BP >/= 140/90 mmHg
unilateral weakness (2 points)
speech disturbance without weakness
duration >/= 60 min (2 points)
Duration 10-59 min
Diabetes
31
What are the two categories of hemorrhagic stroke?
intracerebral hemorrhage and subarachnoid hemorrhage
32
What is the most common cause of ICH?
chronic hypertension
33
What are the 3 "B"s of increased ICP?
Bradycardia, BP increasing, bradypnea
34
What is mannitol dose for increased ICP?
0.25-2 g/kg IV of 15-25% solution over 30-60 minutes
35
If no clinical signs of increased ICP, what should target BP be?
160/90
36
If clinical signs of increased ICP exist, consider ICP monitoring with what goal for CPP?
60-80 mmHg
37
What is the difference between simple partial seizures and complex partial seizures?
Simple partial = brief event WITHOUT alteration of consciousness
complex partial = impairment of consciousness and +postictal state
38
What is a secondary generalized seizure?
partial seizure that spreads to both hemispheres
(eg generalized seizure preceded by aura or unilateral motor symptoms)
38
What is a secondary generalized seizure?
partial seizure that spreads to both hemispheres
(eg generalized seizure preceded by aura or unilateral motor symptoms)
39
What are the two types of nonconvulsive seizures?
absence or petit mal
40
What is seen on EEG during nonconvulsive seizures?
brief 3Hz, spike and wave discharges on EEG
41
what is another name for convulsive seizures?
Grand mal
42
What are the different types of convulsive (grand mal) seizures? List 5
clonic
tonic
tonic-clonic
myoclonic
atonic
43
What is Todd paralysis?
Focal paralysis, typically following a generalized seizure usually lasts 1-2 hours but may last 1-2 days
44
How is status epilepticus defined?
Seizure lasting ≥ 5 minutes
or
≥ 2 discrete seizures without a complete recovery in between the events
45
If seizure due to alcoholism is suspected, which two things should be given (besides benzos)?
thiamine and glucose
46
What are two possible side effects of phenytoin administration?
hypotension and cardiac dysrhythmias (due to its propylene glycol diluent)
47
What is the difference between phenytoin and fosphenytoin?
fosphenytoin is the water soluble prodrug of phenytoin (with better side effect profile)
48
what is the onset of action of phenytoin and fosphenytoin?
10-30 minutes
49
What are possible side effects of phenobarbibtal?
sedation, respiratory depression, and hypotension
50
What is the onset of action of phenobarbital?
15-30 minutes
51
What should be given for seizures in pregnancy?
Magnesium sulfate, if eclamptic
Otherwise, discuss with neuro and OB -- risk of seizures is likely much worse than risk of teratogenicity
52
What should be given if seizure is suspected to be due to isoniazid overdose or gyromitrin toxin (mushroom)?
Pyridoxine (Vitamin B6)
53
What is the most common bacteria implicated in meningitis?
streptococcus pneumoniae
(gram positive diplococci)
54
In meningitis in ages >60 years old, what organism should be considered and covered with antibiotics?
Listeria monocytogenes
(gram-POSITIVE rod)
cover with Ampicillin
55
What are the three most common organisms implicated in meningitis in those <1 month old?
Group B strep
E coli
L monocytogenes
56
What are the three most common causes of meningitis following neurosurgical procedure or head trauma?
S pneumoniae
Staph aureus
Pseudomonas aeruginosa
57
What is the most common viral cause of meningitis and what season is it most common?
Enterovirus
summer months
58
Which 2 organisms should always be considered as cause for meningitis in immunocompromised?
Fungal (eg cryptococcus)
Parasitic (eg Toxoplasma gondii)
59
What are some noninfectious causes of meningitis?
SLE
Drug induced
Carcinomatosis
Sarcoidosis
Behcet disease
60
What does bacterial meningitis typically start?
nasopharyngeal colonization --> hematogenous spread --> CNS infection
61
Meningitis due to fungi typically spread from what source?
Pulmonary
62
What do you call the following physical exam finding?
Position the patient with hips and knees flexed. Extend the knees. Flexion of neck or pain in neck is positive sign.
Kernig sign
63
What do you call the following sign?
Neck flexion results in flexion at hips (neck sign) or passive flexion of hip on one side results in contralateral hip flexion (contralateral sign).
Brudzinski sign
64
What three concomitant infections should you look out for in suspected meningitis?
Sinusitis, otitis, pneumonia
65
When is a Head CT recommended BEFORE LP in suspected meningitis?
1. patients >60 years old
2. immunocompromised (eg HIV)
3. History of CNS disease (stroke, mass lesions, or head trauma)
4. New onset seizures within 1 week
5. Marked CNS depression, papilledema, or focal neuro deficits
66
What are the 3 contraindications to LP?
1. Coagulopathy (relative): INR > 1.5, Platelets <50k (<20k = absolute)
2. infection at skin puncture site (absolute)
3. Increased ICP or trauma to lumbar vertebrae
67
What is normal opening pressure for LP?
5-20 cm H2O
68
What are normal leukocyte levels for CSF?
69
What is a normal CSF protein level?
20-45
70
What is normal glucose for CSF?
50-80% or 60-70% of serum level
71
How does the LP opening pressure change in bacterial meningitis?
elevated
72
How does the LP opening pressure change in viral meningitis?
normal or slightly elevated
73
What is the typical CSF leukocyte count in bacterial meningitis?
>/= 500 leuks/mm3
74
What is the typical CSF leukocyte count in bacterial meningitis?
100-500 leuks/mm3
75
What is the CSF %neutrophil count in bacterial meningitis?
>80%
76
What is the CSF %neutrophil count in bacterial meningitis?
<50%
77
What is the CSF protein level in bacterial meningitis?
>200
78
What is the CSF protein level in bacterial meningitis?
<200
79
What is the CSF glucose level in bacterial meningitis?
80
What is the CSF glucose level in viral meningitis?
usually normal
81
What is the CSF glucose level in fungal meningitis?
<50%
82
What is the CSF protein level in fungal meningitis?
>200
83
What is the CSF %neutrophil level in fungal meningitis?
<50%
84
What is the CSF leukocyte count in fungal meningitis?
10-500
85
What is the LP opening pressure in fungal meningitis?
elevated
86
CSF gram stain with gram positive diplococci suggests what organism?
pneumonoccocus
87
CSF gram stain with gram negative diplococci suggests what organism?
meningococcus
88
CSF gram stain with small pleomorphic gram negative coccobacilli suggests what organism?
H influenzae
89
CSF gram stain with gram positive rods and coccobacilli suggests what organism?
listeria
90
What immediate empiric antibiotics should be given if meningitis suspected?
Vancomycin 1gIV
Ceftriaxone or Cefotaxime 2g IV
+/- Ampicillin if neonate, >60 yrs old, debilitated, or alcoholic
+/- Metronidazole if concern for extension from sinusitis or otitis
91
Giving antibiotics before LP will not decrease ability to detect organism in CSF fluid if LP performed
within ___ hours and antigen assays are utilized
2
92
Should steroids be given for meningitis?
YES-- Appears to decrease morbidity and mortality in adults with bacterial meningitis (especially S pneumoniae) and children with H influenzae
meningitis.
93
What is the dose for steroids for meningitis?
Dexamethasone 0.15 mg/kg IV 15 minutes before or concurrent with the first dose of antibiotics, repeat every 4-6 hours (max 10 mg in adults).
94
What is the treatment for viral meningitis?
no specific treatment unless herpes simplex meningitis -- then acyclovir
95
If neisseria meningitidis or H influenzae type b is identified as cause for meningitis, what should close contacts be treated with?
rifampin (4 doses 10 mg/kg q12h) is recommended
once bacterial organism is identified.
Alternatively, ciprofloxacin can be used (500 mg PO single dose).
96
What is the most common cause of encephalitis?
viruses - majority of cases
Arbovirus and HSV = most common
97
What is the diagnostic imaging of choice for encephalitis?
MRI with contrast
(CT with contrast is alternative but is less sensitive)
98
What is the empiric treatment for encephalitis where HSV or HZV are suspected?
Acyclovir 10mg/kg IV q8h
99
What is the empiric treatment for encephalitis where cytomegalovirus is suspected?
Ganciclovir
100
What are the 3 mechanisms of spread that cause brain abscesses?
1. Contiguous infection of middle ear, sinus, or teeth
2. Neurosurgery or penetrating trauma
3. Hematogenous spread
101
How does a brain abscess appear of MRI/CT with contrast?
ring-enhancing lesions
102
What is the empiric treatment for brain abscesses with no obvious source?
Vancomycin + ceftriaxone or cefotaxime +
metronidazole
103
What is the most common cause of secondary seizures in the developing world?
Neurocysticercosis (CNS T solium larvae
infection -- from eating undercooked pork)
104
What is the treatment for Neurocysticercosis (CNS T solium larvae infection)?
Antiparasitic agents (praziquantel and albendazole).
105
The majority of shunt infections present within _______ (time period) of placement).
within 6 months
(50% within 2 weeks).
106
Which two organisms are most commonly implicated in intracranial shunt infections?
■ Staphylococcus epidermidis (50%)
■ S aureus
107
What percentage of SAH have a completely normal neuro exam?
50%
108
What is the Hunt and Hess classification?
The Hunt and Hess scale is a grading system used to classify the severity of a subarachnoid hemorrhage based on the patient's clinical condition. The scale ranges from a score of 1 to 5. It is used as a predictor of prognosis/outcome with a higher grade correlating to a lower survival rate.
109
How sensitive is a noncon Head CT for identifying SAH?
Symptoms < 24 hours = sensitivity > 90%-95% (controversial, some sources cite 98% within 12 hours). Increasing evidence that the sensitivity
of CT within the first 6 hours after a minor SAH approaches 100%.
Symptoms for 1 week = sensitivity < 50%.
110
What is the gold standard for diagnosing SAH if CT negative?
Xanthochromia (via spectrophotometry, NOT naked eye) ≥ 12 hours after onset of headache
111
In SAH, what should BP goal be?
Control BP (MAP < 130).
112
What medication has been shown to prevent vasospasm and ischemic stroke?
(initiate within 4 days of symptom onset)
Nimodipine PO
113
What is a subdural hygroma?
Collection of blood-tinged fluid in dural space of uncertain etiology; tends to follow trauma; on CT fluid density is same as CSF; surgical evaluation is needed, if symptomatic
114
What is the most common cause of brain tumor?
metastases from lung or breast carcinoma
115
What should steroids be considered for brain mets?
if edema is present on imaging or if severe symptoms
116
What is the diagnosis criteria for Temporal arteritis?
3 of 5 criteria:
■ Age > 50
■ New onset localized headache
■ Temporal artery tenderness or decreased pulse
■ Erythrocyte sedimentation rate > 50 mm/h
■ Refer urgently for temporal artery biopsy to confirm diagnosis if highly suspicious
117
What is the treatment for Temporal Arteritis?
Immediate high dose steroids: Prednisone 40-80 mg/d
NSAIDs for pain relief
118
What is a complication of temporal arteritis?
loss of vision due to ischemic optic neuritis
119
What is idiopathic intracranial hypertension also known as?
Pseudotumor cerebri
120
What are risk factors for idiopathic intracranial hypertension (aka pesudotumor cerebri)?
young obese female
oral contraceptives
vitamin A
chronic steroid use
tetracyclines
and thyroid disorders
121
What are signs/symptoms of idiopathic intracranial hypertension (aka pesudotumor cerebri)?
■ Long-standing headache ± visual disturbances and nausea/vomiting.
■ Visual loss may occur.
■ Eye findings may include papilledema, loss of peripheral vision, and CN VI palsy.
122
How is idiopathic intracranial hypertension (aka pesudotumor cerebri) diagnosed?
increased intracranial pressure (> 25 cm H2O) with
normal CSF evaluation
(Head CT may show small ventricles and an enlarged cisterna magna)
123
When diagnosing idiopathic intracranial hypertension (aka pesudotumor cerebri), what test should be done/what should be excluded?
Consider magnetic resonance venography (MRV) for evaluation of cerebral venous thrombosis
124
What is the treatment for idiopathic intracranial hypertension (aka pesudotumor cerebri)?
Acetazolamide (decreases CSF formation) +/- furosemid
125
When are steroids and/or therapeutic LP indicated for idiopathic intracranial hypertension (aka pesudotumor cerebri)?
In the setting of acute vision loss at temporizing measure until surgical intervention
126
What is the treatment for refractory idiopathic intracranial hypertension (aka pesudotumor cerebri)?
Optic nerve sheath fenestration or shunt placement
127
What are the most common causes of stroke in patients <45 years old?
internal carotid and vertebral artery dissection
(usually due to trauma or injury)
128
What are symptoms of internal carotid dissection?
Unilateral anterior neck pain or headache around the eye or frontal area, classically abrupt in onset.
■ ipsilateral Horner syndrome, contralateral stroke, or TIA symptoms.
Horner syndrome:
partial ptosis (drooping or falling of the upper eyelid), miosis (constricted pupil), and facial anhidrosis (absence of sweating) due to a disruption in the sympathetic nerve supply
129
What are signs/symptoms of vertebral artery dissection?
Marked occipital or posterior neck pain with signs of brainstem TIA or stroke
130
How are internal carotid and vertebral artery dissection diagnosed?
CTA and/or MRI/MRA to confirm diagnosis
(noncon CT is NOT diagnostic study of choice)
131
What is the treatment for internal carotid and
vertebral artery dissection?
1. Surgical
2. Anticoagulation with IV heparin --> warfarin with target INR 2-3
thrombolysis with IV alteplase for eligible patients with acute ischemic stroke
132
In what population is cerebral venous thrombosis most common?
neonates and children
in adults, more common in women
133
What are some causes of cerebral venous thrombosis?
1. adjacent local infection (meningitis or ear, nose, and throat [ENT] infections),
2. direct injury (eg, trauma) or
3. hypercoagulable state (eg, pregnancy, Factor V Leiden, lupus anticoagulant, nephrotic syndrome, cancer).
134
Cerebral venous thrombosis must be considered in any patient with new diagnosis of ____________.
idiopathic intracranial hypertension
135
How is Cerebral Venous Thrombosis diagnosed?
MRV combined with MRI is imaging modality of choice
CT and standard MRI are useful only if positive and CANNOT exclude the diagnosis
CT venography is a rapid, readily available, and accurate technique for detecting cerebral venous thrombosis; use may be limited because of low resolution of the deep venous system and cortical veins
136
What is the treatment for Cerebral Venous thrombosis?
Heparin
If severe --> catheter-based thrombolysis
137
What causes a post-LP headache
persistent CSF leak from the LP puncture site
138
What are the characteristics of post-LP headache?
headache that is worse with upright posture and improved with laying flat
139
What is the treatment for a post-LP headache
simple analgesics
IV fluids
Caffeine IV
if no relief with above --> blood patch (epidural injection of autologous blood)
140
What precautions can be taken to prevent post-LP headache?
1. Use small-bore needle with noncutting tip, angle needle parallel to longitudinal fibers of the dura and reinsert stylet prior to needle removal.
***Bed rest after LP and patient positioning have not been shown to reduce incidence***
141
When does a post LP headache typically occur relative to LP?
within 24-48 hours of LP
142
What is the suspected pathophysiology of a migraine headache?
Hypothesis is related to a slowly spreading wave of neuronal depolarization across the brain → ion dysfunction and vasoconstriction → prodrome and
aura (seen in 20%)
Trigeminovascular activation and release of peptides → inflammation of the pain-sensitive areas and vasodilation.
143
What are some factors thought to trigger migraine headaches?
■ Menstruation, contraceptive estrogens, pregnancy
■ Certain foods or drinks, such as chocolate, caffeine, hard cheese, alcoholic beverages (especially red wine), monosodium glutamate (MSG), nitrites
■ Alterations in circadian rhythm
144
What is the difference between a "common migraine" and a "classic migraine"?
common migraine = migraine without aura
classic migraine = migraine WITH aura
145
What is the most common type of aura associated with a classic migraine?
visual = most common
- scintillating scotomata or visual field deficit
146
How is an ophthalmoplegic migraine defined?
Headache + CN 3, 4, 6 deficits
147
How is a retinal migraine defined?
headache + sudden monocular blindness
148
What is the mechanism of action of triptans in the treatment of migraines?
Selective 5-HT (Serotonin) agonists
- cause vasoconstriction and blocks peptide release = decreased inflammation and pain
149
When are Triptans contraindicated?
Patients with hypertension or other cardiovascular disease (because they are potent vasoconstrictors)
(do not use within 24 hours of other ergotamine-containing medications)
150
What is the mechanism of action of dihydroergotamine (DHE, aka Migranal) in the treatment of migraines?
Nonselective 5-HT agonist
151
When is dihydroergotamine (DHE, aka Migranal) contrainidicated?
Those with cardiovascular disease or within 24 hours of triptan use
or if you are taking any of the following medications: antifungals such as itraconazole, ketoconazole; HIV protease inhibitors such as indinavir (Crixivan), nelfinavir (Viracept), and ritonavir (Norvir); or macrolide antibiotics such as clarithromycin (Biaxin), erythromycin (E.E.S., E-Mycin, Erythrocin), and troleandomycin (TAO).
152
What are common side effects of dihydroergotamine (DHE, aka Migranal)?
Nausea and vomiting
153
What anti-emetics are best in migraines?
prochlorperazine, metoclopramide
154
What population is prochlorperazine contraindicated?
older adults with dementia taking antipsychotics
155
Nausea and vomiting are proposed to arise from peripheral or central stimulation of serotonin type 3 (5-HT3) and dopamine type 2 receptors, the predominant receptors expressed at the ___________ (part of the brain).
chemoreceptor trigger zone (CTZ)
156
chemoreceptor trigger zone (CTZ) is also commonly known as what?
Area postrema
157
Where is the chemoreceptor trigger zone (CTZ) (aka Area Postrema) located?
located within the dorsal surface of the medulla oblongata, on the floor of the fourth ventricle of the brain
158
What is the utility of steroids in migraine headaches?
parenteral dexamethasone (10-24mg IV) is effective for reducing the rate of migraine recurrence (but not immediate relief)
159
What is a common side effect of metoclopramide?
Tardive dyskinesia
160
What medications are used for migraine prevention?
initial treatment with amitriptyline, venlafaxine, one of the beta blockers (metoprolol or propranolol), or topiramate.
161
Describe characteristics of tension-type headaches.
bilateral, non-pulsating, not worsened by exertion
usually not associated with nausea and vomiting
162
What is the treatment for tension-type headaches?
NSAIDs
for severe headache --> treat same as migraine
163
In what population are cluster headaches most common?
young to middle aged men
164
What are common precipitates of cluster headaches?
alcohol and stress
165
Cluster headaches result from dysfunction of the ____ nerve.
trigeminal
166
What are characteristics of Cluster headaches?
severe, unilateral orbital, supraorbital, or temporal pain;
episodes last 15-180 minutes, but recur in clusters (daily on same side for weeks)
167
What are some symptoms associated with headache in cluster headaches?
Associated ipsilateral findings:
■ Conjunctival injection, lacrimation, nasal congestion, rhinorrhea, facial swelling, miosis, or ptosis
168
What is the most effective treatment of cluster headaches?
High flow O2 is effective in 70% of patients
(7-12L via NRB)
169
Besides O2, what are some other treatments for cluster headaches?
■ IV dihydroergotamine or sumatriptan; oral preparations take too long to
be effective.
■ Prophylaxis with oral steroid burst, verapamil, or antiepileptic agents (carbamazepine,
phenytoin).
170
What are the three categories of confusional states (AMS)?
1. delirium
2. dementia
3. psychosis
171
What are the signs/symptoms of delirium?
■ Acute confusional state
■ Transient attention and cognition impairment
■ Waxing and waning symptoms
■ Hallucinations, if present, are visual and/or auditory
172
What is the treatment for delirium?
treat underlying cause & be attentive to needs, sleep patterns, reorientation and redirection
Sedate with Haloperidol or benzos if severe agitation as a last resort as these meds can worsen delirium
173
What is the most common cause of dementia?
Alzheimer disease
174
What is the pathophysiology of Alzheimer disease?
Reduction of neurons in the cerebral cortex and increased amyloid deposition → neurofibrillary tangles and plaques
175
What are examples of treatable causes of dementia?
■ Depression (most common treatable cause)
■ Vitamin B12 deficiency
■ Neurosyphilis
■ Hypothyroidism
■ Normal pressure hydrocephalus
■ Intracranial mass (eg, brain tumor)
■ Chronic drug use
176
How is dementia diagnosed?
Diagnosis is primarily based on history of slow, progressive change in behavior.
All patients warrant neuroimaging, thyroid-stimulating hormone (TSH), and vitamin B12 level at minimum.
177
What examination can be used test cognitive impairment and screen for dementia?
Mini-mental state examination
178
Which six categories does the mini-mental state exam test?
1. orientation
2. memory
3. attention
4. calculation
5. recall
6. Language
179
What score on the MMSE identifies cognitive impairment?
Cutoffs of < 24 or < 25 out of 30 are used to identify cognitive impairment
180
What are two medications used in the treatment of Alzheimer disease?
donepezil (Aricept) and tacrine (Cognex)
reduce the metabolism of acetylcholine
181
How is vascular dementia treated?
treat risk factors (hypertension)
182
What causes normal pressure hydrocephalus (NPH)?
results from defective CSF uptake
(either a primary process or secondary to prior infection/injury/bleed)
leading to increased CSF volume
183
What is the triad of signs/symptoms seen in NPH?
1. dementia
2. ataxia
3. Urinary frequency or incontinence
(wacky wobbly wet)
184
How is NPH diagnosed?
Based on CT showing ventricular enlargement (without other pathology) and LP with normal intracranial pressure and fluid studies.
185
What is the treatment for NPH?
Neurosurgical consultation for shunt placement.
186
What are signs and symptoms of psychiatric psychosis?
■ Loss of contact with reality.
■ Hallucinations, if present, are auditory.
■ Usually not waxing and waning.
■ Consciousness not clouded.
187
Consciousness can be divided into ____ and ___ functions.
arousal and content
188
Arousal functions reside in the ___________ in the midbrain, pons, and medulla.
reticular activating system (RAS)
189
Content functions reside in the ______ .
cerebrum
190
_____ represents a failure in both arousal and content functions of the brain
Coma
191
What is the mnemonic for causes of coma?
TIPS AEIOU
Trauma, temperature
Infection
Psychiatric, poisonings
Space occupying lesion, subarachnoid
Alcohol
Epilepsy, electrolytes, encephalopathy
Insulin
Opioids/overdose, oxygen (hypoxia, CO2 narcosis)
Uremia (metabolic)
192
What is the oculovestibular reflex?
(Also known as caloric stimulation)
Direction of FAST component of nystagmus,
with irrigation of cold versus warm water
in patient with intact brainstem:
COWS
Cold
Opposite
Warm
Same
With ICED WATER -- as consciousness is lost, the FAST component (towards the non-irrigated ear) is lost and the slow component deviates the eye in the direction of the irrigated ear.
193
What is the oculocephalic reflex?
Oculocephalic reflex:
ensure the C-spine is cleared.
With patient's eyes open, the head is briskly turned from side to side with the head held briefly at the end of each turn.
a POSITIVE response occurs when the eyes rotate to the opposite side to the direction of head rotation, thus indicating that the brainstem (CN3,6,8) is intact.
a similar result is seen when the head is flexed and extended — a positive result is downward deviation of the eyes during extension, and upward deviation during flexion (the eyelids, if closed, may also open as part of the ‘doll’s head phenomenon’).
These vertical responses indicates that the brainstem (CN3,4,8) is INTACT.
The eyes should gradually return to the mid-position in a smooth, conjugate movement if the brainstem is intact.
Patients with metabolic coma (e.g. hepatic failure) may have exaggerated, brisk oculocephalic reflexes.
194
How is ataxia defined?
failure to make smooth, intentional movements
195
What are the two types of ataxia?
MOTOR (CEREBELLAR) ATAXIA
SENSORY ATAXIA
196
How does location of lesion within cerebellum affect incoordination?
lateral cerebellar lesion --> limb incoordination
midline cerebellar lesion (vermis) --> axial incoordination
197
Describe a cerebellar ataxic gait.
wide based with unsteady and irregular steps
198
Describe a sensory ataxic gait.
abrupt movement of legs and slapping of feet with each step
199
What is dysmetria?
inaccurate fine movements
200
What is dysdiadochokinesia?
clumsy rapid movements
201
What is dyssynergia?
breakdown of movements into parts
202
What is Romberg test?
Worsened unsteadiness with eyes closed (loss of visual input) is suggestive of SENSORY ataxia. If unsteadiness present with patient’s
eyes open, consider cerebellar pathology.
203
How is nystagmus named directionally?
The direction of nystagmus is named by
the fast (cortical) component.
204
How is vertigo defined?
the perception of movement where no movement exists
205
Describe nystagmus that would suggest a central cause of vertigo.
Vertical and bi-directional (direction changing) nystagmus
206
What are some other symptoms associated with vertigo that may suggest posterior fossa pathology?
diplopia, dysarthria, visual changes
207
What is the imaging study of choice to visualize the posterior fossa (cerebellum, medulla, and pons)?
MRI
(CT may miss up to 80% of posterior cerebrovascular accidents (CVAs))
208
What are some characteristics that more commonly suggest peripheral causes for vertigo?
1. dramatic and sudden onset
2. +n/v
3. positional
4. rotatory-vertical or HORIZONTAL nystagmus
5. hearing loss
6. no central findings
209
What test, if positive, confirms posterior canal BPPV?
Dix-Hallpike test
210
Describe the Dix Hallpike test.
1. The patient begins sitting up, head oriented 45 degrees toward the ear to be tested.
2. Lay patient down quickly with head past the end of the bed and extends their neck 20 degrees below the horizontal, maintaining the initial rotation of the head.
3. Watch the patient's eyes for torsional and up-beating nystagmus, which should start after a brief delay and persist for no more than one minute.
This would indicate a positive test.
211
What are some characteristics of central vertigo?
classically ill defined and constant
vertical nystagmus
212
What are some characteristics of central vertigo?
classically ill defined onset (rather than sudden onset) and constant
VERTICAL nystagmus
213
What is the pathophysiology of BPPV?
Otoconia in the semicircular canals
214
What is the pathophysiology of Meniere disease?
Increased endolymph within the chochlea and labyrinth
215
What is the pathophysiology of Labyrinthisis?
viral or bacterial infection
216
What is the pathophysiology of Ramsay-Hunt Syndrome (vestibular ganglionitis)?
viral infection of vestibular ganglion
217
What are the signs/symptoms of Ramsay Hunt syndrome?
Hearing loss, vertigo, facial nerve palsy, grouped vesicles
218
What is the pathophysiology of perilymph fistula?
trauma, sudden pressure change
219
What are common causes of CN VIII lesions?
schwannomas, meningioma
220
What are characteristics of CN VIII lesions?
gradual onset of vertigo, preceded by hearing loss
221
Which five muscles does the Oculomotor Nerve (CN III) supply?
1. levator muscle of the eyelid
2. medial rectus muscle
3. superior rectus muscle
4. inferior rectus muscle
5. inferior oblique muscle
also constricts the pupil through its parasympathetic fibers
222
What physical exam findings suggest an oculomotor nerve palsy?
lid ptosis
mydriasis (a "blown" pupil)
then "down and out" eye
223
What muscle is innervated by the Trochlear Nerve (CN IV)?
Superior Oblique muscles
-- deficit results in vertical diplopia
224
What are the three anatomic divisions of the trigeminal nerve (CN V)?
V1 - ophthalmic
V2 - maxillary
V3 - mandibular
225
What are signs/symptoms of trigeminal neuralgia?
1. brief, recurrent episodes of excruciating, unilateral facial pain lasting only seconds
2. Right more than left side predominance
3. May be able to elicit pain by tapping the side of the face, otherwise there should be no demonstrable physical findings
226
What is the treatment for trigeminal neuralgia?
Carbamazepine and analgesics
(will need outpatient follow up to monitor carbamazepine levels, CB, and LFTs)
227
Which muscle is innervated by the Abducens Nerve (CN VI)?
Lateral rectus muscle
228
Describe an Abducens nerve (CN VI) palsy.
diplopia due to unopposed action of the medial rectus muscle; affected eye is pulled medially
diplopia is worse with lateral gaze towards the affected eye
229
What is the most common cause of CN VI impairment?
diabetic neuropathy
230
What is the most common cause of Bell Palsy?
Herpes virus infection
(pregnant women are at greater risk)
231
In addition to facial paralysis, what other findings are seen in Bell palsy?
loss of taste of anterior 2/3s of tongue
hyperacusis (sound distortion or tinnitus)
bell phenomenon: eye appears to roll back in head when patient attempts to close the lid
232
What is the treatment for ramsay hunt syndrome?
prednisone;
controversial -- acyclovir for severe cases
233
What organism is implicated in malignant otitis externa?
pseudomonas (especially if diabetic or immunocompromised)
234
What are symptoms of an acoustic neuroma?
hearing loss accompanying facial weakness
(Schwannoma of CN VIII)
Classic triad:
1. hearing loss
2. tinnitus
3. disequilibrium
235
What is the test of choice for diagnosing an acoustic neuroma?
MRI
236
What is the treatment for Bell Palsy?
if within 1 week of symptoms:
- corticosteroids
- antiviral therapy
Eye protection, artificial tears
237
Which tract contains motor pathways and has its fibers cross in medulla then descend in the spinal cord?
Corticospinal tract
238
Which tract contains pain and temperature pathways and has its fibers first cross then ascend in the spinal cord?
Spinothalamic tract
239
Which part of the spinal cord contains vibration and proprioceptive pathways and has its fibers ascend in ipsilateral spinal cord to medulla, then crosses?
Posterior (dorsal) columns
240
What part of the spinal cord contains lumbar and sacral nerve roots?
Cauda equina
241
How does damage to upper motor neurons affect reflexes?
decreased reflexes initially, then hyperreflexia after several days
242
How does damage to lower motor neurons affect reflexes?
decreased reflexes
243
What are classic findings of Central Cord Syndrome?
Bilateral motor weakness of upper extremities > lower extremities
&
distal > proximal extremities
244
What is the likely mechanism of injury Central Cord Syndrome?
Hyperextension injury of narrowed cervical spinal
canal
245
What are classic findings of Brown-Sequard injury?
Ipsilateral motor weakness and vibration/
position loss
Contralateral pain and temperature loss
246
What is the likely mechanism of injury Brown-Sequard Syndrome?
Pentrating trauma
247
What are classic findings of Anterior Cord Syndrome?
Motor weakness,
Loss of pinprick and light touch.
Preserved vibration and position sense
248
What is the likely mechanism of injury Anterior Cord Syndrome?
Infarction of Anterior Spinal Artery
249
What are classic findings of Cauda Equina Syndrome?
Urinary retention (overflow incontinence),
decreased rectal tone, saddle anesthesia,
motor weakness
250
What is the likely mechanism of injury Cauda Equina Syndrome?
Ruptured L4-5 disc
251
What are the signs/symptoms of discitis?
Back pain, fever, and refusal to walk in child < 10 y
252
What is the likely etiology of discitis?
Inflammatory process in disc (viral or
Staphylococcus aureus)
253
What are the signs/symptoms of Dorsal column disorders?
Loss of position sense, vibration, and light touch
254
What is the likely etiology of Dorsal column disorders?
Syphilis or vitamin B12 deficiency
255
What are the signs/symptoms of HIV myelopathy?
Weakness, gait problems, spasticity, sphincter dysfunction
256
What is the likely etiology of HIV myelopathy?
Advanced HIV
257
What are the signs/symptoms of spinal epidural abscess?
Severe pain with radiation down spine, signs of cord
compression, fever
ESR elevated
Get MRI (or if unavailable, CT myelogram)
258
What is the likely etiology of Spinal epidural abscess?
Expanding abscess (IDU or
immunocompromise)
259
What are the signs/symptoms of Spinal epidural hematoma?
Severe pain with radiation down spine, signs of cord
compression
260
What is the likely etiology of Spinal epidural hematoma?
Expanding hemorrhage (trauma/procedures or
coagulopathy)
261
What are the signs/symptoms of syringomyelia?
Dissociative anesthesia (loss of pain and temperature sensation with preservation of proprioception and light touch),
weakness, spasticity, interosseous wasting of hands
262
What is the likely etiology of syringomyelia?
Syrinx formation in central spinal cord
(usually seen in cervical spine in association with Arnold-Chiari malformation)
263
What are the signs/symptoms of transverse myelitis?
Transverse level of sensory loss, paresis,
sphincter dysfunction
264
What is the likely etiology of transverse myelitis?
Post-viral or toxic inflammation
265
What is the pathophysiology of Guillain-Barre Syndrome (GBS)?
an acute demyelinating disorder of the peripheral nerve
Antecedent illness (viral or Campylobacter jejuni gastroenteritis, upper respiratory infection [URI]) → autoimmune response → damage to myelin sheath → symptoms
266
hat are signs and symptoms of Guillain Barre Syndrome?
antecedent illness --> latent period
ascending symmetric paresthesias and motor weakness (peaks within 3 weeks of onset)
decreased DTRs
normal rectal tone
may progress to ventilatory failure
267
What is the Miller Fisher Variant of Guillain Barre Syndrome?
Ophthalmoplegia, ataxia, ↓ or absent reflexes.
Around 25% will have limb weakness in addition to cranial nerve/cerebellar findings.
268
How is Guillain Barre Syndrome diagnosed?
Electrodiagnostic testing -- nerve conduction studies (NCS) and electromyography (EMG)
CSF = markedly elevated protein (>45 ug/dL) with up to 100 lymphocytes/uL
269
What is the treatment for Guillain Barre Syndrome?
Supportive therapy
IVIG or plasmapheresis
Respiratory, FEV1, NIF monitoring
270
What organism causes diptheria?
Corynebacterium diptheriae
271
What is the pathophysiology of diptheria?
Respiratory or skin (tropical climates or poor hygiene) infection with
C diphtheriae → exotoxin release →
■ Local membrane formation
■ Peripheral neuropathy → neurologic symptoms
272
What disease classically causes Exudative pharyngitis with progressive weakness?
Diptheria
273
How is diptheria treated?
Diptheria antitoxin
+abx (penicillin or erythromycin)
274
What causes diabetic distal symmetric polyneuropathy?
microvascular injury to the nerve
275
What is the treatment for diabetic polyneuropathy?
duloxetine, pregabalin, and the capsaicin patch [8%]
276
What is the treatment for radial mononeuropathy?
Splint wrist in 60° of dorsiflexion
277
What is the treatment for ulnar mononeuropathy?
Corticosteroid injection may help.
May require surgical intervention if persistent.
278
What is the treatment for median mononeuropathy?
■ Wrist splinting in neutral position
■ Corticosteroid injection into carpel tunnel
■ Oral corticosteroid burst
■ Release of flexor retinaculum for severe symptoms
279
What is the treatment for sciatic and common fibular mononeuropathy?
Splint ankle at 90° with posterior splint
280
How is mononeuropathy multiplex defined?
characterized by the presence of multiple
mononeuropathies
asymmetric
281
What is the most common cause of mononeuritis multiplex?
diabetes mellitus
282
How is mononeuropathy multiplex diagnosed?
■ Electrodiagnostic studies
■ Sural nerve biopsy if diagnosis in question
283
_________________________ is a disorder characterized by upper motor neuron disease in addition to lower motor neuron pathology.
Amyotrophic lateral sclerosis (ALS)
284
What is the pathophysiology of Amyotrophic lateral sclerosis (ALS)?
■ Anterior horn cell neuronopathy → peripheral nerve findings
■ Loss of Betz cells in the CNS motor cortex → upper motor neuron findings
285
What are the signs and symptoms of Amyotrophic lateral sclerosis (ALS)?
LMN involvement:
- muscle fasciculations and atrophy
- muscle cramps
- asymmetric distal weakness
UMN involvement:
- hyperreflexia and clonus
- spasticity
- positive babinski
286
How do people with Amyotrophic lateral sclerosis (ALS) typically die?
progressive respiratory muscle weakness (→ respiratory failure) or dysphagia (→ aspiration). ↑ risk with forced vital capacity < 25 mL/kg
287
How is ALS diagnosed?
electrodiagnostic testing
288
What is the treatment for ALS?
supportive
Riluzole -- modulates glutamate metabolism
289
What is the pathophysiology of myasthenia gravis?
Antibodies against acetylcholine receptors at the neuromuscular junction → destruction of receptors → decrease in available receptors
290
How does the muscle fatigue of MG compare to that of Lambert Eaton syndrome?
Repeated muscle use increases weakness (vs Lambert-Eaton myasthenic syndrome where repeated muscle use improves strength).
291
What is acute myasthenic crisis?
respiratory failure requiring mechanical
ventilation
triggers include infection, medications
292
What 3 things should be on your differential for ptosis?
myasthenia gravis
CN3 palsy
Horner Syndrome
293
What is the Edrophonium (Tensilon) test?
■ Edrophonium is a short-acting acetylcholinesterase blocking agent
→ increased acetylcholine available at neuromuscular junction
→ improvement in measured ptosis (and other symptoms).
■ Test dose must be administered first to ensure that cholinergic crisis will not be induced. Cholinergic crisis from excess anticholinesterase
inhibitors can present with flaccid paralysis and is difficult to distinguish from myasthenic crisis.
■ Have atropine ready in case of excessive cholinergic symptoms.
294
What is the treatment of MG?
Cholinesterase inhibitors
■ Pyridostigmine, neostigmine.
■ Should NOT be used during myasthenic crisis!
■ Excessive administration → cholinergic crisis with weakness, tachycardia, excessive secretions, etc.
295
What is Lambert Eaton Myasthenic Syndrome commonly associated with?
About half the time it is associated with cancer (small cell carcinoma of the lung, lymphoma).
296
What is the pathophysiology of Lambert-Eaton Myasthenic Syndrome?
Antibodies → inadequate release of acetylcholine at neuromuscular junctions → symptoms
297
What are the signs and symptoms of Lambert Eaton Myasthenic Syndrome?
■ Proximal (primarily leg) muscle weakness that improves with repeated stimulation
■ Autonomic symptoms (dry mouth, impotence)
298
What is the treatment for Lambert Eaton Myasthenic Syndrome?
■ Treat underlying malignancy, when present.
■ Immunosuppressive agents.
■ Plasmapheresis and IVIG, if severe.
299
What is the pathophysiology of botulism?
Toxin produced by Clostridium botulinum → presynaptic inhibition of acetylcholine release at the neuromuscular junction.
300
How is botulism diagnosed?
■ Clinical suspicion
■ Electrodiagnostic testing
■ Botulinum toxin testing of serum and stool
301
What is the pathophysiology of Tick Paralysis?
Tick toxin → decreased release of acetylcholine at neuromuscular junction → symptoms
302
What are symptoms of Tick Paralysis?
Symmetric ascending paralysis
Tx: remove tick
303
What are the two types of inflammatory myopathies?
Polymyositis and dermatomyositis
304
What is the difference between polymyositis and dermatomyositis?
Both cause:
■Chronic symmetric proximal muscle weakness.
■ Muscle pain and tenderness.
But, Dermatomyositis has additional skin findings, including photosensitivity and extensor rashes.
305
How are polymyositis and dermatomyositis diagnosed?
Electromyography and muscle biopsy confirm diagnosis.
306
How are polymyositis and dermatomyositis treated?
Oral prednisone or cytotoxic drugs
307
What disease is caused by regions of CNS demyelination with sparing of axons?
Multiple Sclerosis
308
What are risk factors for MS?
females are 3x more likely
Caucasians are 2x more likely than AAs
309
What is internuclear ophthalmoplegia? (as seen in MS)
Abnormalities in eye adduction bilaterally
associated with horizontal nystagmus
310
What is Uhthoff phenomenon (associated with MS)?
Small increases in body temperature (eg, exercise,
fever) → worsened symptoms (visual symptoms often most affected).
311
What is Lhermitte phenomenon?
Electric shock sensation down spine with flexion
of neck (common with all cervical myelopathies (disc bulge, spinal stenosis, etc)
312
Describe CSF findings of MS?
CSF cell counts, protein, and glucose are typically normal;
CSF may show oligoclonal bands of IgG and/or myelin-based proteins
313
What is the treatment for MS?
■ High-dose methylprednisolone burst with taper for acute exacerbations
■ β-Interferon, azathioprine
314
What do you call the chronic neurodegenerative disease of the elderly resulting from damage to dopaminergic neurons in the substantia nigra?
Parkinson Disease
315
What are the 4 characteristic findings of Parkinson Disease?
■ Resting tremor (“pill-rolling”)
■ Cogwheel rigidity
■ Bradykinesia or akinesia
■ Postural instability
"TRAP"
Tremor
Rigidity
Akinesia
Postural instability
316
How is Parkinson Disease diagnosed?
Based on clinical findings
CT/MRI is not definitive
317
What is the treatment for Parkinson Disease?
Agents to increase CNS dopamine and anticholinergics to decrease central
muscarinic activity
(Drug “holidays” of 1 week may be used as effectiveness diminishes over time.)
318
Which medications are used for acute migraine treatment?
1. triptans
2. dihidryergotamines
3. NSAIDs
4. Acetaminophen
5. Antiemetics
319
What medications are used for migraine prevention prophylaxis?
1. Beta blockers (propanolol)
2. Calcium channel blockers (verapamil)
3. Tricyclic antidepressants (amitriptyline)
4. Anticonvulsants (valproic acid, topiramate)
5. Calcitonin gene-related peptide receptor antagonists
6. Botulinum toxin A
320
How is degree of cerebral edema evaluated on a noncontrast head CT?
estimating the density ratio of gray to white matter
This density is measured in Hounsfield units. Normally, the gray to white matter density ratio is 1:3.
In cerebral edema (the result of hypoxic-ischemic injury), this ratio is decreased
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