Neurology Flashcards
Define stroke
Sudden onset of a neurological deficit from the death of brain tissue
Risk factors for stroke
HTN
DM
Hyperlipidemia
Tobacco
Same as those for MI
Weakness/sensory loss
Homonymous hemianopsia
+/- Aphasia
MCA stroke (more than 90% of cases)
- Weakness/sensory loss on the contralateral side of the lesion
- Loss of visual field on the opposite side of the stroke w/ eyes looking towards the side of the lesion
- Aphasia if the stroke occurs on the same side as the speech center
Personality/congitive defects (e.g., confusion)
Urinary incontinence
Leg > arm weakness
ACA stroke
Sensory loss of the face
Sensory loss of the limbs on the opposite side
Limb ataxia
PCA stroke
- Ipsilateral sensory loss of the face
- Contralateral sensory loss of the limbs
The best initial therapy for a nonhemorrhagic stroke is:
< 3 hours since onset = thrombolytics
> 3 hours = ASA
Patient presents 6 hours after the onset of a nonhemorrhagic stroke and is currently taking aspirin daily, what is your initial therapy?
Add dipyridamole
or
Switch to clopidorgrel
Every patient with a stroke should be started on what type of long-term medication?
Statin (regardless of LDL)
True/False
Carotid angioplasty and stenting are of proven value for stroke patients
False
It is always a wrong answer
When is endarterectomy indicated?
> 70% stenosis of the carotid
If the stenosis is 100% no intervention is needed (no point in opening a passage that is 100% occluded)
Headache:
Bilateral “bandlike” pressure
Lasts 4-6 hours
Normal physical exam
Tension headache
Treat with NSAIDs and Acetaminophen
Headache:
Aura w/ photophobia
Related to food/emotions/menses
Migraine
Treat by avoiding triggers, taking NSAIDs and triptans (5-HT1 agonists)
When is prophylaxis indicated for migraine headaches and what is it?
When attacks occur 3 or more times per month
Propranolol or
Sodium valproate
Headache:
Episodic pain
Unilateral
Lacrimation
Eye reddening
Nasal stuffiness
Cluster headache
Treat with sumitriptan, octreotide, or oxygen
Prophylatic treatment for cluster headaches
Verapamil
or
Prednisone
or
Sodium valproate
What else should you evaluate for when someone presents with signs/symptoms of a cluster headache (specifically headache + red eye)?
Glaucoma
How do you diagnose pseudotumor cerebri?
Diagnosis cannot be made without a CT or MRI to exclude an intracranial mass lesion and a lumbar puncture (LP) showing increased pressure
Associated with obesity, venous sinus thrombosis, OCPs, and vitamin A toxicity
Look for papilledema with diplopia from 6th cranial nerve palsy (mimics brain tumor)
Treatment for pseudotumor cerebri
Wt loss + acetazolamide (decreases production of CSF)
Steroids help
Repeated LPs
Last resort = shunt or fenestrate the optic nerve
First step if someone is suspected of having Giant cell arteritis
Critical to start steroids without waiting for biopsy
Look for visual disturbance, systemic symptoms, and jaw claudication
Markedly elevated ESR
Difference in abortive therapy for migraine and cluster headache
Both can be interrupted with either ergotamine (5-HT1, DA, and NE) or one of the triptans (5-HT1)
Only cluster headaches respond to 100% oxygen, prednisone, and lithium
What is the best prophylatic therapy for migraines?
Propranolol
Treatment for trigeminal neuralgia?
Carbamazepine or oxcarbazepine
If unimproved by meds, gamma knife surgery
How to reduce the incidence of postherpetic neuralgia?
Treatment with antiherpetic medications
Steroids DO NOT help
Treatment for postherpetic neuralgia?
TCAs
Gabapentin
Pregabalin
Carbamazepine
Phenytoin
Topical capsaicin
Define epilepsy
Seizures of unclear etiology
Angina is to MI, as confusion is to:
coma and seizure
What is status epilepticus?
Status epilepticus (SE) is an epileptic seizure of greater than five minutes or more than one seizure within a five-minute period without the person returning to normal between them.
Treatment for Status Epilepticus
- Benzodiazepine
- Fosphenytoin
- Phenobarbital
- General anesthesia
Why is fosphenytoin preferred over phenytoin?
Fewer adverse effects
Phenytoin in a class 1b antiarrhythmic (when given IV it is associated with hypotension and AV block)
Indications for long-term treatment of a seizure
Status Epilepticus
Focal neurological signs
Abnormal EEG or lesion on CT
FHx of seizures
Best treatment for epilepsy
Unclear
Levetiracetam, phenytoin, valproic acid, and carbamazepine all have nearly equal efficacy (Levetiracetam has the fewest adverse effects)
Ethosuximide is the best for absence seizures
When can you discontinue antiepileptic drugs?
When the patient has been seizure-free for 2 years
Sleep deprivation EEG is the best way to tell if there is possibility of recurrence (lacks high sensitivity)
Polycystic kidney disease
Tobacco
HTN
Hyperlipidemia
High alcohol consumption
Look out for aneurysms (i.e., SAH)
Severe headache
Stiff neck and photophobia
Fever
SAH
How does SAH differ from meningitis
SAH = very sudden in onset with LOC
and
normal WBC to RBC ratio
How to diagnose SAH
Best initial test = CT without contrast
Most accurate = LP showing blood (only necessary for the 5% that have a falsely negative CT scan)
Normal WBC to RBC ratio is 1:500-1000
Treatment for SAH
Nimodipine (CCB): prevents subsequent ischemic stroke
Embolization: better than surgical clipping at preventing repeated hemorrhage
Shunt: only if hydrocephalus develops
Seizure prophylaxis: phenytoin
Best initial therapy for bacterial meningitis
Ceftriaxone and vancomycin
Best initial test for brain abscess
head CT or MRI
Cancer and infection are indistinguishable based on imaging; biopsy is essential
Empiric therapy for suspected brain abscess
Penicillin (vancomycin if indicated)
+
Ceftriaxone (or cefepime)
+
Metronidazole
Neurological abnormalities
Adenoma sebaceum
Shagreen patches
Ash leaf patches
Retinal lesion
Cardiac rhabdomyomas
Tuberous Sclerosis
No specific treatment, control seizures
Soft, flesh-colored lesions attached to peripheral nerves
Cafe au lait spots
Neurofibromatosis Type I (von Recklinghausen disease)
Eighth cranial nerve lesions may need surgical decompression to help preserve hearing
Port-wine stain of the face
Seizures
Sturge-Weber Syndrome
Tremor at rest and with exertion
Improved with alcohol
Worse with caffeine
Essential Tremor
The best therapy is propranolol
Define parkinsonism
loss of cells in the substantia nigra resulting in a decrease in dopamine
PArkinson’s Disease = doPAmine Down
Alzheimer’s Disease = ACh Down
Why is postural instability (aka orthostatic hypotension) seen with parkinsonism
The same slowness that results in bradykinesia (slow movements) results in the inability of the pulse and blood pressure to reset appropriately
Treatment of mild Parkinson’s
Anticholinergic medications (benztropine and trihexyphenidyl)
Amantadine (definitely the answer in patients > 60 who are intolerant of anticholinergic adverse effects)
Treatment for severe Parkinson’s
DA agonists (pramipexole and ropinirole) = best initial therapy
Levodopa/carbidopa = most effective
COMT inhibitors (tolcapone, entacapone) = extended duration of levodopa/carbidopa and decreased on/off phenomena
MAO inhibitors (rasagiline, selegiline)
Deep brain stimulation
Which medication for Parkinson’s has the only possibility of retarding the progression of the disease?
MAO inhibitors
Rasagiline and selegiline
Shy-Drager syndrome
Parkinsonism predominantly with orthostasis
Define spasticity
painful, contracted muscles from damage to the CNS
often associated with MS
Treat with baclofen, dantrolene, or tizanadine
Treatment for Restless Leg Syndrome
Pramipexole (DA agonist)
- Iron supplementation if deficient*
- Gabapentin or Ropinorole are alternatives*
CAG trinucleotide repeat sequences on chromosome 4
Huntington Disease
Treatment for Huntington Disease
Dyskinesia is treated with tetrabenazine (reversible depletion of DA, 5-HT, and histamine from nerve terminals)
Psychosis is treated with haloperidol or quetiapine
Treatment for Tourette Disorder
Fluphenazine, clonazepam, or pimozide
Associated with ADHS (treat with methylphenidate)
Define MS
Idiopathic disorder of CNS white matter
What is internuclear ophthalmoplegia (INO)?
the inability to adduct one eye with nystagmus in the other eye
INO is characteristic of MS
Diagnostic tests for MS
Best initial test = MRI
LP is only the answer in the 3-5% of patients with an equivocal or nondiagnostic MRI (looking for oligoclonal bands)
Treatment for MS
High-dose steroids (shortens the duration of MS exacerbations)
Glatiramer and beta-interferon are the best first choice for prevention of relapse
A patient with MS develops worsening neuro deficits with the use of a chronic suppressive medication. MRI shows new, multiple white matter hypodense lesions. What happened?
Likely taking Natalizumab (also used for Crohn’s), which has been associated with the development of PML
Weakness of unclear etiology
Difficulty chewing and swallowing
Decrease gag reflex
ALS
Weakness
Spasticity
Hyperreflexia
Extensor plantar responses
UMN lesion
Weakness
Wasting
Fasciculations
LMN lesion
Treatment for ALS
Riluzole reduces glutamate buildup and may prevent progression
Baclofen treats spasticity
CPAP and BiPAP help with repiratory difficulties (will ultimately need tracheostomy and maintenance on a ventilator)
Most common cause of peripheral neuropathy
DM
Best initial treatment is pregabalin or gabapentin
Difference in presentation between stroke and Bell Palsy
If the patient can wrinkle their forehead on affected side = stroke
If the patient cannot wrinkle their forehead on the affected side = Bell palsy
Hyperacusis
Taste disturbances
Features of Bell’s Palsy
Hyperacusis because the 7th cranial nerve normally acts as a “shock absorber” on the ossicles of the middle ear
Taste disturbances because the 7th cranial nerve supplies the sensation of taste to the anterior 2/3 of the tongue
Treatment for Bell’s Palsy
60% of patients have full recovery without treatment
The best initial therapy is prednisone
What is the most common complication of Bell’s palsy?
Corneal ulceration
7th cranial nerve palsy makes it difficult to close the eye on the affected side, leading to dryness and ulceration
Which infection is Guillain-Barre Syndrome associated with?
Campylobacter jejuni
Ascending weakness
+
Loss of reflexes
GBS
Diagnostic tests for GBS
Most specific = nerve conduction/electromyography (takes 1-2 weeks to become abnormal)
CSF will show increased protein and a normal cell count
PFTs are the most important initial test (decrease in FVC is the earliest way to detect impending respiratory failure)
Best initial test for Myasthenia Gravis
Acetycholine receptor antibodies
- For patients without these, get anti-MUSK antibodies (muscle-specific kinase)
- Edrophonium test
- Most accurate = electromyography
Treatment for Myasthenia Gravis
Neostigmine or pyridostigmine
If unimproved, thymectomy in patients < 60 and prednisone if > 60
