neurology Flashcards
(178 cards)
1
Q
tension headache character
A
30 minutes to 7 days Typically bilateral location Pressure or tight quality Does not prohibit activity Not associated with nausea
2
Q
tension headache tx
A
Treat acute headache with NSAIDs
A tricyclic antidepressant may be needed for prophylaxis
3
Q
trigeminal neuralgia symptoms
A
Brief paroxysms of unilateral lancinating pain in the V2 or V3 distribution of the trigeminal nerve, often
triggered by light touch of the affected area
4
Q
imaging needed for trigeminal neuralgia
A
MRI to rule out intracranial lesions and MS
5
Q
tx for trigeminal neuralgia
A
Select carbamazepine for treatment
6
Q
medication overuse headache symptoms
A
Chronic headache that occurs ≥10 days per month in patients using combination analgesics,
ergotamine products, or triptans; chronic headache that occurs >15 days per month in patients using
simple analgesics
7
Q
chronic migraine characteristics
A
Headache occurring ≥15 days per month for >3 months
Headache possessing the features of migraine ≥8 days per month
Risk factors include migraine headache frequency or acute medication use >10 days per month
8
Q
1st and 2nd line tx for migraisn
A
nsaids
then use triptans if lack of response or severe
9
Q
treatment for . Migraine that is present on awakening, is associated with vomiting, or is found to escalate rapidly
A
intranasal triptans or subcutaneous
10
Q
tx for migraine assoc nausea
A
Metoclopramide and prochlorperazine
11
Q
indications to use prophylaxis for migraine
A
migraines do not respond to therapy
• headache occurs ≥10 days per month
• disabling headache occurs ≥4 days per month
• use of acute migraine medications is >8 days per month
12
Q
options for ppx tx of migraines
A
amitriptyline, metoprolol, propranolol, timolol,
topiramate, valproic acid, and venlafaxine. Onabotulinum toxin A is indicated in chronic migraine.
13
Q
contraindications to triptans
A
CAD and cerebrovascular disease, brainstem aura, and hemiplegic migraine.
14
Q
characteristics of cluster headaches
A
Pain usually periorbital, duration 15-180 minutes, several times per day. Repeating over weeks then
disappearing for months or years. Unilateral tearing and nasal congestion or rhinorrhea, eyelid
edema, miosis and/or ptosis
15
Q
tx of cluster headaches
A
acute - triptan and oxygen
chronic veramapil
16
Q
symptoms of chronic paroxysmal hemicranias
A
Occurs at least five times daily lasting 2-30 minutes. Responds completely to indomethacin.
17
Q
Short-lasting Unilateral Neuralgiform headaches with Conjunctival injection and Tearing
A
Dozens to hundreds of times per day, with durations of 1 to 600 seconds. Typically resistant to treatment.
18
Q
Hemicrania continua symptoms
A
Persistent strictly unilateral headache that responds to indomethacin
19
Q
red flag symptoms for headache (9)
A
- first or worst headache
- abrupt onset or thunderclap attack
- progression or fundamental change in headache pattern
- abnormal physical examination findings
- neurologic symptoms lasting >1 hour
- new headache in persons >50 years old
- new headache in patients with cancer, immunosuppression, or pregnancy
- association with alteration in or loss of consciousness
- headache triggered by exertion, sexual activity, or Valsalva mane
20
Q
testing for headaches when red flag symptoms are present
A
MRI over CT in nonemergency situations
• CT for suspected acute ICH
• ESR or CRP for suspected giant cell arteritis
• LP for suspected infectious or neoplastic meningitis or disorders of intracranial pressure
21
Q
Subarachnoid hemorrhage
(SAH) clues
A
Sudden onset of “worst headache of my life”
Many patients have warning “sentinel” headaches
before SAH
22
Q
carotid or vertebral dissection clues
A
Neck pain and ipsilateral headache; neurologic
findings in territory of involved vessel
tx with asa heparin or anticoag
23
Q
clues for thrombosis of cerbral vein or dura sinus
A
Exertional headache, papilledema, neurologic
findings
Consider in hypercoagulable states, pregnancy, use of
oral contraceptives
Tx LMWH followed by warfarin
24
Q
Reversible cerebral
vasoconstriction syndrome clues
A
Recurrent thunderclap headache syndrome, more
frequent in women. Associated with pregnancy,
neurosurgical procedures, exposure to adrenergic or
serotonergic drugs. Imaging shows strokes,
hemorrhages, or cerebral edema
25
Idiopathic intracranial hypertension (pseudotumor cerebri) is
characterized by
intracranial pressure without identifiable structural pathology. Patients are typically female, obese, and
of child-bearing age. Papilledema is nearly always present.
26
diagnose and tx pseudotumor cerebri
Diagnosis is confirmed by a CSF pressure >250 mm H2O with normal fluid composition. MRI may be normal or show small ventricles, widened optic nerve sheaths, or a partially empty sella.
tx acetazolamide
27
epilepsy diagnosis
two or more unprovoked seizures occurring more than 24 hours apart or one unprovoked seizure with a significant ongoing risk of further unprovoked seizure
28
Focal seizure without alteration of awareness
| (formerly simple partial seizures) charateristics
Normal consciousness and awareness
Single neurologic modality (sensory, motor, olfactory, visual, gustatory) involving a
single region of the body, such as the hand or arm
29
Focal seizure with alteration of awareness
| (formerly complex partial seizure) characteristics
Conscious but unresponsive or staring
Automatism (lip smacking, swallowing, or manipulating objects)
Postictal confusion
30
Primary generalized seizure characteristics
Loss of consciousness or awareness at onset
No prodromal or localizing symptoms
Whole-body stiffening (tonic) and/or jerking (clonic) seizures
31
Temporal lobe epilepsy
Focal seizures with alteration of awareness preceded by an aura before losing consciousness. Often unaware that they have become impaired and may have no recollection of the seizure. Medial temporal sclerosis is a characteristic finding on MRI.
32
Idiopathic (genetic)
| generalized epilepsy
Any combination of tonic-clonic seizures, absence seizures, and myoclonic seizures. MRI typically normal. EEG may show generalized spike-wave abnormality.
33
Frontal Lobe epilepsy
Nocturnal complex seizures that awaken patients from sleep. Often associated with underlying structural
pathology (e.g., tumor, vascular malformations).
34
Myoclonic seizure
A generalized seizure associated with brief, lightning-like jerks of the arms, not associated with loss of
consciousness (misdiagnosed as “jitteriness”).
35
Convulsive status epilepticus
Characterized by continuous seizure for ≥5 minutes. Most common cause is low AED level. Complications
include aspiration pneumonia, fever, hemodynamic instability, acidosis, PE, and rhabdomyolysis;
associated with a mortality rate of approximately 20%.
36
symptoms of PNES
* forced eye closure
* long duration
* hypermotor activity that starts and stops
* pelvic thrusting
37
evaluation needed after first unprovoked seizure
• EEG (although a normal EEG does not rule out a seizure)
• CBC, electrolyte and glucose levels, and toxicology screen
• brain MRI (or head CT in an emergency)
• CSF examination if the patient has fever, prolonged altered mental status after the seizure, is immunosuppressed, or has
a severe headache
38
how do you diagnose PNES and what population is susceptible to pNES
Inpatient video EEG monitoring is required to make the diagnosis of PNES
PTSD in military
39
carbamazepine SE
interactions with other hepatically metabolized drugs and increased risk for osteoporosis and
hypercholesterolemia
40
• valproic acid SE
weight gain, hypercholesterolemia, PCOS, teratogenicity, hepatotoxicity
41
tompiramate and zonisamide SE
increased risk of kidney stones
42
• carbamazepine and oxcarbazepine SE
hyponatremia, pancytopenia
43
all AED have a potential SE of
drug hypersensitivity syndrome, SJS, and suicidal ideation
44
when can you stop AED
seizure free for 2-5 years
45
AEDs that are relatively safe in preg
lamotrigine (dose adjustment)
| and levetiracetam
46
most common cause of status epileticus
low blood AED levels
47
tx for status epilepticus
First-line treatment is IV lorazepam, IV diazepam, or IM midazolam. Patients not taking AEDs should then be treated with phenytoin or fosphenytoin, administered after
5 minutes of continuous seizing
48
when is Surgical clipping or endovascular coiling of aneurysms are indicated
patients with aneurysms ≥7 mm in the posterior circulation or ≥12 mm in the anterior circulation.
49
all patients with TIA require
* emergent head CT without contrast (to rule out intracranial hemorrhage)
* ECG and telemetry or event monitoring (to rule out AF)
* vascular studies (cerebrovascular ultrasonography or cerebrovascular MRA, CTA)
* echocardiography (to rule out LV or valvular thrombus
50
abcd2 scoring system
Age ≥60 y 1
Blood pressure ≥140/90 mm Hg 1
Clinical Symptoms
• focal weakness with the TIA 2
• speech impairment without weakness 1
Duration of TIA
• ≥60 min 2
• 10-59 min 1
Diabetes mellitus present 1
51
what abcd2 score do you hospitalize
>/=3
52
what kind of stroke should you consider in older adults with persistent, acute-onset vertigo
vertibral basilar
53
how quickly do you need to administer tpa
within 3 hours or 4.5 hrs in selective patients
54
exclusion criteria for tpa
* age >80 years
* severe stroke
* diabetes mellitus with a previous infarct
* anticoagulant use
increased risk of bleeding, diagnosis of ICH, or SBP
>185 mm Hg and DBP >110 mm Hg
55
additional stroke treatment acutel
* treat temperature >38.0 °C (100.4 °F) with acetaminophen
* administer normal saline to maintain euvolemia
* give aspirin, 325 mg, unless thrombolysis is planned
* start DVT prophylaxis within 48 hours
56
only times to start antihypertensive therapy early in acute stroke instead of permissive htn
* SBP is >220 mm Hg, DBP is >120 mm Hg, or MAP is >140 mm Hg
* thrombolytic therapy is planned, and SBP >185 mm Hg or DBP >110 mm Hg
* ACS, aortic dissection, or end-organ damage is present
57
whats considered a small SAH
<7 mm posterior or <12 mm anterior circulation can be monitored by MRI
58
most common location/cause of SAH
results from the rupture of saccular (“berry”) aneurysms of the circle of Willis.
59
eye symptoms in SAH
(third nerve palsy and dilated pupil
60
what should you do if SAH is suspected but CT negative
Do CSF to look for erythrocytes or xanthochromia.
61
Tx for SAH
• Treat ruptured aneurysms with surgical clipping or endovascular coiling within 48 to 72 hour
• Maintain BP <140/80 mm Hg to prevent rebleeding.
• Select oral nimodipine for 21 days to prevent vasospasm and improve
neurologic outcomes.
62
what needs to be done in the setting ICH and cocaine use
Cerebral angiography is indicated for patients <45 years of age with ICH related
to cocaine use
63
what score on mini mental is associated with dementia
<24
64
routine testing/imagining for dementia
Routinely obtain brain imaging with CT or MRI to detect nondegenerative causes that would alter management, such as cerebrovascular disease, neoplasm, subdural hematoma, or hydrocephalus. Screen all patients for depression.
65
when to obtain LP in dementia
* rapidly progressive dementia
* age of onset <60 years
* history of malignancy or paraneoplastic disorders
* suspicion for acute or subacute infection; immunosuppressed or immunodeficiency state
* positive syphilis or Lyme serology
* systemic autoimmune disease; suspected CNS autoimmune or inflammatory disorder
66
diagnose Gradual memory loss, aphasia, apraxia, agnosia, inattention, and decrease in
executive function
alzheimer disease
67
diagnose: Imaging or history positive for stroke responsible for impairment of at least
one cognitive domain
Common findings include focal neurologic findings, depression, pseudobulbar
palsy, gait abnormalities, and urinary difficulties
vascular neurodegenerative disorder
68
Mild parkinsonism characterized by postural instability and gait difficulty,
fluctuating cognition, delusions, and visual hallucinations
dementia with lewy body
69
Early and prominent personality changes, behavioral disturbances including
disinhibition and impulsivity, diminished frontal and/or temporal lobes on MRI,
onset before age 60 years
Frontotemporal dementia, behavioral variant
70
Dementia, shuffling gait, urinary incontinence, and ventriculomegaly in the
absence of past history of meningitis, SAH, or trauma
Normal-pressure hydrocephalus
71
Choreoathetosis and dementia, autosomal dominant pattern of
| inheritance
Huntington disease
72
Prominent myoclonus, characteristic EEG pattern of triphasic sharp waves, CSF
protein 14-3-3, rapidly progressive onset at early age
Creutzfeldt-Jakob disease
73
Early postural instability and falls, apathy, parkinsonism poorly responsive to
levodopa, and vertical gaze palsy
Progressive supranuclear palsy
74
History of head injury followed by delayed development (10 years) of
impaired concentration, short-term memory, executive dysfunction, and
judgment; aggression, depression, irritability, violent behaviors, and
suicidality; and parkinsonism, unsteady gait, shuffling gait, and slurred speech
Chronic traumatic encephalopathy
75
treatment for mild to mod dementia
(donepezil, rivastigmine, and galantamine)
76
side effects of ach inhibitors
bradycardia, diarrhea, heart block, nausea and vomiting, and syncope
77
best option to delay cog decline in moderate alzheimer
Memantine
78
tx for lewy body
ach inhibitors
79
tx for normal cephalic hydrocephalus
large volume LP
80
parkinsons cause
degeneration of dopaminergic neurons in the substantia nigra of the midbrain
81
parkinsons diagnosis requires 2 of the following
bradykinesia (slowed movement and decreased amplitude of repetitive movement)
• rigidity (cogwheel type)
• resting tremor (or with movement)
• postural reflex abnormality (falling)
82
Early dementia within the first year of the appearance of parkinsonism is a
hallmark of
dementia with Lewy bodies.
83
early signs of parkinsons
loss of smell, constipation, and acting out dreams may
| precede the onset of motor symptoms by years
84
cutaneous associatio with parkinsons
sebhoreic dermatitis
85
Multiple system atrophy
Severe orthostatic hypotension and ataxia
| MRI showing “necrosis” of the putamen and cerebellar atrophy
86
Progressive supranuclear palsy
```
Unexplained falls (typically backward), inability to move eyes vertically, and parkinsonian
features
```
87
Medication-induced parkinsonism
Antiemetics (prochlorperazine, metoclopramide), antipsychotics (haloperidol),
reserpine, lithium, and methyldopa
88
what are some concerns of levadopa and how to counteract them
associated with motor fluctuations,
including dyskinesias, and a “wearing-off” effect (enhanced parkinsonian symptoms). Initiating therapy with a dopamine
agonist (pramipexole, ropinirole) in patients younger than 65 years avoids the early appearance of these side effects
89
side effects of dopamine agonist
sedation and an increase in compulsive behaviors such as gambling, shopping, and
hypersexuality
90
manifestations of Essential tremor
Typically slowly progressive or stable over time
Bilateral postural or kinetic tremor; improves with alcohol
Family history positive in 50%
91
treatment for essential tremor
Propranolol, primidone, or topiramate
92
manifestation of huntingtons
Most common neurodegenerative cause of generalized
chorea
Also progressive dementia and psychiatric
manifestations
Autosomal dominant
93
tx for huntingtons
Symptomatic treatment with
| tetrabenazine and deutetrabenazine
94
manifestations of Drug-induced dystonia
Tardive dyskinesia associated with choreiform and
dystonic craniofacial movements
Can be caused by neuroleptic, antiemetic, and
serotoninergic medications
95
tx for drug induced dystonia
Stop the offending drug
Valbenazine, clonazepam, tetrabenazine,
anticholinergic agents, and clozapine`
96
Cervical dystonia (torticollis) manifestations
Cervical muscle contractions resulting in abnormal
| posture of the head and neck
97
Cervical dystonia (torticollis) treatment
Botulinum toxin (first line)
98
Tourette syndrome manifestations
Childhood onset, multiple complex motor tics, and
| presence of vocal tics (e.g., echolalia)
99
Tourette syndrome treatment
Reassurance or cognitive behavioral
| therapy
100
Myoclonus manifestations
Rapid, shock-like, jerky movements of isolated body parts
Underlying metabolic disorder, serotonin syndrome,
postanoxic, Creutzfeldt-Jakob disease, corticobasal
degeneration
101
myoclonus treatment
Treat the underlying metabolic disorder
102
what should you screen patients <40 years with “essential tremor” or dystonia for
Wilson disease with serum ceruloplasmin and
| 24-hour urine copper measurements.
103
what is MS
episodes of dysfunction resulting from demyelinating lesions (plaques) in different areas of the CNS
(brain, brain stem including optic nerve, or spinal cord) at different times.
104
what is Relapsing-remitting MS
Clinical episodes of neurologic dysfunction, typically lasting weeks before improving, that may lead
to the accumulation of disability.
105
what is Secondary progressive disease in MS
Disappearance of evidence of clinical relapses in the relapsing-remitting form and by
progressive disability.
106
what is Primary progressive MS disease
Progressive disability accumulation from the time of disease onset.
107
Optic neuritis description
Subacute visual deficit in one eye along with pain with eye movement
108
Afferent pupillary defect MS involvement
Paradoxical dilation of the pupil when light is rapidly shifted from the
unaffected to the affected eye
109
Papillitis MS involvement
Inflammatory changes in the retina causing a flared appearance of the optic
disc
110
Myelitis MS involvement
Focal inflammation within the spinal cord manifesting as sensory, autonomic,
or motor symptoms below the affected spinal level
111
Lhermitte sign MS involvement
A shock-like sensation radiating down the spine or limbs induced by neck
movements
112
Bladder MS involvement
Urinary frequency, urgency, or retention
113
Cerebellum MS Involvement
ataxia and vertigo
114
Brainstem MS involvement
(internuclear ophthalmoplegia) Inability to adduct one eye and nystagmus in the abducting eye
115
Uhthoff phenomenon in MS
Transient worsening of baseline neurologic symptoms with elevations of body
temperature
116
how to diagnose MS
evidence of CNS demyelination disseminated in both space and time as demonstrated through a combination
of documented clinical relapses, signs on physical examination, and the distribution of lesions on an MRI.
117
CSF finding in MS
oligoclonal IgG bands or an elevated IgG index
118
Treatment of MS flare
IV methylprednisolone followed by oral glucocorticoids speeds recovery from acute exacerbations, most effectively in acute
optic neuritis.
Treat fever and look for underlying cause of fever before starting steroids
119
chronic treatment for MS after first flare
interferon beta or glatiramer acetate if imaging suggests MS.
120
what vitamin is helpful additive for MS patients
Vitamin D added to interferon beta reduces the accumulation of MRI lesions and is recommended for all patients with MS
121
Tx for r confirmed relapsing-remitting MS (RRMS).
Prescribe interferon beta or glatiramer acetate
122
MS Spasticity tx
Physical therapy, stretching, massage therapy
Baclofen, benzodiazepines, cyclobenzaprine,
tizanidine
123
MS Neuropathic pain
Carbamazepine, duloxetine, gabapentin,
| pregabalin, topiramate
124
MS Fatigue tx
Proper sleep hygiene, regular exercise
Amantadine, amphetamines, armodafinil,
modafinil
125
MS Depression tx
Individual or group counseling
| Antidepressants (SNRIs, SSRIs)
126
MS cognitive dysfunction tx
Cognitive rehabilitation and accommodation
strategies
No medication has been proven effective
127
MS mobility tx
Physical and occupational therapy; use of braces,
canes, rolling walkers, or electrostimulatory walkassist devices
Dalfampridine
128
MS Urinary retention tx
Manual pelvic pressure, intermittent catheterization
129
• Interferon agents are contraindicated in patients with ...
Liver disease or depression
130
is getting pregnant with MS increase risk of disability
NO
131
does Combining glatiramer acetate with interferon beta provide greater therapy
NO
132
what is Neuromyelitis optica
| Devic disease
Recurrent episodes of myelitis and optic neuritis without the brain lesions typical of MS; NMO-IgG
autoantibody may be present
133
what is Idiopathic transverse
| myelitis
Subacute onset of weakness, sensory changes, and bowel/bladder dysfunction, typically after a viral infection
Distinguished from MS by the presence of complete myelitis, no oligoclonal bands or elevated IgG index in
the CSF, and no lesions on brain MRI
134
b12 myelopathy characteristics
Paresthesias, lower-extremity weakness, and gait instability
Findings may include paraparesis, vibration and position sense loss, and sensory ataxia.
Anemia may be absent
135
Copper deficiency myelopathy characteristics
Mimics vitamin B12 deficiency
| May develop after bariatric surgery or from excessive zinc ingestion
136
Infarction of the spinal
| cord characteristics
Acute onset of flaccid paralysis or weakness and pinprick sensation loss below the level of the infarction
Potential causes include emboli, hypotension during cardiovascular/aortic surgery, and AV malformations
137
```
Clues to the cause of compression myelopathy:
• fever
• anticoagulation
• cancer
• trauma
• elderly with chronic back/leg pain
```
* fever — epidural abscess
* anticoagulation — epidural hematoma
* cancer — metastases
* trauma — vertebral fracture
* elderly with chronic back/leg pain — spinal stenosis
138
tx for transverse myelitis
IV methylprednisolone
139
Spinal cord compression caused by leukemia, lymphoma, myeloma, and germ cell tumors may be treated urgently with surgery or radiation?
radiation!
140
signs of ALS
combination of upper motoneuron signs (e.g., hyperreflexia, spasticity, and extensor plantar
response) coexistent with lower motoneuron findings (e.g., atrophy and fasciculation). Sensory deficits are characteristically absent.
141
how does ALS symptoms present
Muscle weakness in patients with ALS usually begins distally and asymmetrically, although 20% of patients have bulbar-onset
ALS with difficulty speaking and swallowing
142
tx for ALS
Riluzole may increase survival by about 3 months. Begin noninvasive ventilatory support for patients with respiratory insufficiency. Placement of a percutaneous endoscopic gastrostomy tube is indicated when weight loss or swallowing difficulty occurs.
143
cause of myasthenia Gravis
antibodies directed against the acetylcholine receptor, which results in impaired neuromuscular transmission.
144
signs of MG
ptosis or diplopia (first manifestation in most patients)
• muscle weakness, including dysphagia and dyspnea
• positive anti–acetylcholine receptor antibody titer (found in 90% of patients; negative titer does not rule out MG)
• normal deep tendon reflexes and sensation
• decremental response to repetitive stimulation on EMG
145
Difference between botulism and MG
cranial nerve involvement, including diplopia, dysphagia, and sluggish or nonreactive pupils, whereas the pupils are normal in MG
146
Lambert Eaton symptoms
progressive proximal weakness and diminished tendon reflexes that improve
with repetitive movement of affected muscles
147
diagnosing lambert eaton
Diagnosis is confirmed by detection of serum anti–voltage-gated calcium channel
antibodies and the EMG finding of facilitation of motor response to rapid repetitive stimulation.
148
what disease is lambert eaton associated with
SCLC
149
how to diagnose MG
Single-fiber EMG can establish the diagnosis. Look for elevated serum TSH levels because of the association of MG with autoimmune thyroid disorders. Perform CT of the chest to detect thymoma.
150
what drugs can precipitate MG crisis
aminoglycosides, quinolones, magnesium, β-blockers, or
| calcium channel blockers as precipitants of myasthenic crisis
151
Treatment for MG
pyridostigmine
| Thymectomy if thymoma present
152
Tx for MG crisis
plasmapheresis or IV immune globulin.
| Pyridostigmine monotherapy should be avoided in this scenerio due to increased resp secretions
153
diagnosis: Isolated anterolateral thigh numbness
| without weakness
```
Meralgia paresthetica (a compressive neuropathy
of the lateral femoral cutaneous nerve)
```
Tx: Locate and relieve pressure
154
diagnosis Sensory loss over palmar surface of first
three digits and weakness with thumb
abduction and opposition
Median neuropathy (carpal tunnel syndrome)
155
Diagnose: Numbness of the fourth and fifth fingers
| and weakness of interosseous muscles
Ulnar neuropathy
Tx: Elbow splinting or elbow pads
156
Diagnose: Pain, tingling, and numbness in great toe
| and along medial foot
Tarsal tunnel syndrome
Tx Local glucocorticoid injection;
decompression surgery if severe
157
Diagnose Upper and lower face weakness
Bells Palsy
Tx: Prednisone within 72 hrs
158
Painful, Multiple, noncontiguous nerve deficits
| mononeuritis multiplex
Vasculitis
159
diagnose: Distal and symmetric (stocking-glove)
| sensory or sensorimotor
Axonal polyneuropathies; diabetes and alcohol
| are the most common causes;
160
diagnose Severe unilateral leg pain, numbness,
proximal weakness, atrophy, and weight
loss
dm amyotrophy
161
Diagnose: , ascending, areflexic paralysis and
paresthesias often preceded by GI
illness (usually Campylobacter infection);
CSF shows elevated protein and a
normal cell count (albuminocytologic
dissociation)
Guillain-Barré syndrome
Tx Plasma exchange or IV immune
globulin
Dont do steroids may slow recovery
162
Diagnose: Progressive proximal motor and sensory
neuropathy that evolves over months.
Initial EMG and CSF findings similar to
Guillain-Barré syndrome
Chronic inflammatory demyelinating
polyneuropathy
Prednisone, plasma exchange, or IV
immune globulin
163
Diagnose: Symmetric distal sensory neuropathy in
the setting of MGUS, multiple myeloma,
amyloidosis, and cryoglobulinemia
Paraproteinemic neuropathy
164
How to differentiate myopathy from neuropathy
Myopathies typically present with symmetric weakness of the proximal muscles.
• Normal sensory and reflex examination differentiates myopathy from neuropathy.
• Serum CK level is elevated and falls in response to treatment.
• EMG confirms the presence of myopathic changes (low amplitude, short duration, and polyphasic motor unit potentials)
165
Type of myopathy: Diffuse myalgia, proximal muscle weakness, delayed relaxation phase of deep tendon reflexes, and
elevation of CK
Hypothyroid myopathy
166
Type of Myopathy: Myopathy, brisk reflexes, fasciculation, and ophthalmoplegia
Hyperthyroidism
167
Type of Myopathy: Proximal muscle weakness, myalgia, fatigue, and osteomalacia-related bone pain
Vitamin D deficiency
168
Type of Myopathy: Proximal weakness and myalgia, normal CK levels, and normal EMG findings
Glucocorticoid myopathy
169
type of myopathy: Subacute toxic myopathy associated with rhabdomyolysis
statin myopathy
170
Type of myopathy: Myotonia (manifested as delayed hand-grip release) and distal weakness
Myotonic dystrophies
171
which statins are more likley to cause myopathy
Lipophilic statins (atorvastatin, simvastatin, and lovastatin) have a higher propensity to cause statin myopathy
172
characteristics of meningioma
benign
. CT scan of the head will show a partially calcified, homogeneously
enhancing extra-axial mass adherent to the dura and an enhancing dural “tail.”
Tx resect growing or symptomatic meningioma
173
common primary source for lung met
evaluate the patient for lung cancer, breast cancer,
| and melanoma.
174
Parenchymal metastases on MRI
multiple, ring-enhancing, centrally necrotic lesions
175
What kind of brain met is likely in leukemia and lymphoma
leptomeningeal metastases
176
first line tx for parynchamal or leptomeningial tumor
Glucocorticoids are a first-line treatment for parenchymal and leptomeningeal tumors.
177
initial therapy for patients with leptomeningeal metastases from leukemia and lymphoma
Chemotherapy (methotrexate and cytarabine)
178
cardinal features of brain death
coma, absence of brain stem reflexes, and apnea.
