Neurology Flashcards
In which patients do you perform a head CT scan before lumbar punction when suspect meningitis?
- Papilledema
- Immunocompromised state
- New-onset seizure (within one week of presentation)
- History of CNS disease (mass lesion, stroke, focal infection)
- Abnormal level of consciousness
- Focal neurologic deficit
Most effective method to diagnose dural sinus thrombosis and findings on it
Cerebral venogram→bilateral infarcts along the posterior and anterior frontal lobes and parietal lobes, extending into the white matter (Sagital sinus infarcts)
*Example: Sagital sinus infarcts tend to cross arterial vascular territories and extend into the white matter
Other tests rather than the best initial one that can provide information about myasthenia gravis
- Iced pack test (bedside)➡Application of an ice pack over the eyelids may improve symptoms
- Tensilon test➡Edrophonium (anticholinesterase inhibitor)▶rapidly reverses symptoms
- Abnormal single-fiber EMG and/or a decremental response to repetitive nerve stimulation
Important features to recognize dementia with Lewy bodies
- Visual hallucinations
- Spontaneous parkinsonism
- Fluctuating cognition
- REM sleep behavior disorder
What is Ramsay-Hunt syndrome?
Herpes zoster oticus➡reactivation of VZV in geniculate ganglion➡disrupting VII CN motor fibers, subsequent spread to VIII CN▶painful, erythematous, vesicular rash in auditory canal or auricle; ipsilateral facial paralysis; vestibular (vertigo, nausea/vomiting), hearing, taste disturbances.
What is multiple system atrophy (Shy-Drager syndrome)?
- Parkinsonism
- Autonomic dysfunction (orthostatic hypotension, erectile dysfunction, incontinence, disturbance bowel control, abnormal salivation, lacrimation and sweating, gastroparesis, etc.)
- Widespread neurological signs (cerebellar, pyramidal, lower motor neuron)➡bulbar dysfunction and laryngeal stridor may be fatal
Where is the stroke localization in a patient having right hemiparesis (with hyperreflexia) and left upper and lower facial weakness?
Left pons
*Left CN VI or VII palsy (LMN pattern facial weakness)
Best initial test and their results when suspect idiopathic intracranial hypertension
- MRI→Normal or empty sella (70%)
- MRV→Normal
- Lumbar puncture→Opening pressure >250 mmH2O
Typical MRI/CT finding of high-grade (ex, IV grade) astrocytoma (glioblastoma)
Butterfly appearance with central necrosis, heterogenous serpiginous contrast enhancement
Neuropsychiatric manifestations of Wilson disease
- Psychiatric→Depression, personality changes, psychosis, mania, anxiety
- Neurologic→parkinsonism, dysarthria, choreoathetosis, ataxia
Risk factors of Multiple Sclerosis
- Female, caucasian, HLA-DRB1
- Location: USA, Europe, cold climate
- Low Vitamin D levels
- Smoking
- EBV
Diagnostic and therapeutic (short-term) maneuver for cervical radiculopathy
Shoulder abduction test➡improve radicular symptoms when hand is placed on the top of the head
Ptosis, “down-and-out” gaze, diplopia and normal pupillary response in a patient with poorly controlled diabetes mellitus
Ischemic oculomotor (CN III) palsy [Diabetic ophthalmoplegia]
*Damage to the inner somatic nerve fibers while sparing the more peripheral parasympathetic fibers
Medications that may precipitate myasthenic crisis
- Antibiotics: aminioglycosides, fluoroquinolones
- Beta-blockers
- Calcium channel blockers
- Magnesium
Ulnar nerve neuropathy differences between wrist and elbow level injury
- Wrist➡numbness, paresthesia at medial side of the hand + intrinsic hand weakness (“clumsiness”) [hypothenar, medial lumbrical, adductor pollicis]
- Elbow➡⬇grip strength [flexor carpi ulnaris, medial portion of flexor digitorum profundus]
How you may differentiate guillain-barré syndrome vs tick paralysis?
- GBS➡Autonomic dysfunction in 70% of patients (tachycardia, urinary tract retention, arrhythmias). CSF with albuminocytologic dissociation (⬆proteins, ⬇cells). Ascending symmetrical paralysis over days to weeks.
- Tick-borne paralysis➡Ascending paralysis over hours to days, may be localized or more pronunced on 1 extremity. Look for and find the tick (next best step)
Etiology of tick-borne paralysis
Neurotoxin release: tick needs 4-7 days for neurotoxin release
*Remove the tick➡improvement in an hour, complete recovery in several days (Dermacentor app, Ixodes holocyclus)
Most common adolescent- and adult-onset muscular dystrophy and mode of genetic transmission
- Classic myotonic dystrophy
- Autosomal dominant➡CTG repeat expansion on the DMPK gene
Main clinical presentation of classic myotonic dystrophy
- Progressive skeletal muscle weakness➡face and distal extremities (forearms, hands, ankle flexors)▶muscle wasting➡ptosis, temporal wasting, limb muscle atrophy
- Grip myotonia (hand)
- Dysphagia
- Conduction anomalies
- Testicular atrophy/infertility
Which clinical manifestations might raise suspicion of cervical myelopathy?
- Lower motor neuron (LMN) signs (Ex, weakness and atrophy) at the level of the lesion (arms)
- Upper motor neuron (UMN) signs (Ex, hyperreflexia) below the level of the lesion (legs)
Most common cause of cervical myelopathy in older adults
Spondylosis➡canal narrowing➡spinal cord compression
Most important side effects of phenytoin
- Phenytoin➡❌folic acid absorption in jejunum▶folic acid deficiency over weeks or months
- Megaloblastic anemia
- Gingival overgrowth/hyperplasia
- Phenytoin➡❌bone and mineral metabolism (⬇bone density): calcium and vitamin D supplementation
Symptoms of papilledema due to increased intracranial pressure
- Momentary vision loss that varies according to changes in head position
- Large blind spot in visual fields
Treatment alternative for Parkinson disease when tremor is the dominant symptom and bradykinesia/rigidity are not significant
Anticholinergic therapy (Trihexyphenidyl)
*Limited to younger patients (≤65)→risk of adverse effects in older patients
Ocular manifestations of Neurofibromatosis type 1
- Optic pathway glioma (15% of patients, age<6)➡asymptomatic or grow large to compress optic nerve▶⬇visual acuity, ❌color vision, optic nerve atrophy, proptosis, esotropia, optic disc pallor
- Lisch nodules➡pigmented iris hamartomas
Most common psychiatric complication of multiple sclerosis
Depression
Clinical presentation of anterior spinal artery syndrome
Motor weakness, loss of pain and temperature sensation below the lesion
*Proprioception and vibratory sensation are spared
Clinical presentation of Transverse myelitis
Rapidly progressive myelopathy:
- Motor weakness→from flaccid to spastic paralysis (UMNS)
- Autonomic dysfunction→bowel/bladder incontinence or retention, sexual dysfunction
- Sensory dysfunction→Pain, paresthesia, numbness with distinct sensory level (Ex, lowest spinal cord level with intact sensation). Proprioception and vibration compromised.
Findings on the most useful studies for Transverse myelitis
- MRI→Enhancement of =>1 contiguous spinal cord segments, usually in thoracic cord without evidence of compression
- Lumbar puncture→CSF pleocytosis, elevated IgG
Description of clinical presentation of cluster headache
- Acute onset of unilateral retro-orbital pain (excruciating, sharp, steady)
- Paroxysms onset during sleep, awakening, rapid peak, duration 90 minutes, 8 times daily, 6-8 weeks, remission up to 1 year
- Redness of ipsilateral eye, tearing, nasal congestion, flushing, no visual changes
- Ipsilateral Autonomic manifestations, “Horner Sx like”→ptosis, miosis, anhidrosis
Treatment of acute attacks and prophylactic treatment of cluster headache
- Acute attacks: 100% Oxygen, subcutaneous sumatriptan
- Prophylactic: Verapamil, Lithium
Clinical presentation of cervical myelopathy
- Neck pain radiating to occipital region
- Extremity weaknes and numbness
- Usually first➡Gait dysfunction
- UMN signs (legs)➡slowly progressive spastic quadriparesis, hyperreflexia, Babinski sign, Hoffman sign (corticospinal tract lesion)
- LMN signs (arms)➡muscle atrophy, hyporeflexia
- Sensory changes➡⬇proprioception/vibration/pain sensation in hands or feet
- Respiratory dysfunction
What is the critical illness polyneuropathy?
Axonal injury of peripheral nerves➡weakness after prolonged stay in ICU (Ex, hyporeflexia)
*Complication of sepsis
Which temperature change might trigger multiple sclerosis symptoms?
High environmental temperatures
*Address with cooling techniques
Pharmacologic treatment for frequent/daily restless leg syndrome symptoms
- First line: α2δ calcium channel ligands→Pregabalin, Gabapentin
- Second line: dopamine agonists➡pramipexole, ropinirole, rotigotine, cabergoline
- Last resource: Benzodiazepines (clonazepam), Opioids (codeine)
Most reliable finding to differentiate between epileptic seizure and syncope
Tongue bitting - 32% sensitivity, 96% specificity
*Lateral bitting is even more specific. Frontal bitting might happen in syncope
EEG finding in Creutzfeldt-Jacob disease
Triphasic periodic sharp-wave complexes.
Clinical features that highly suggest cord compression
- Sensory level
- Vertebral tenderness
- Hyperreflexia
Most common causes of cord compression
- Malignancy
- Infection (epidural abscess)
Best first step when cord compression is suspected through clinical findings
Glucocorticoids➡⬇pressure on the cord
In which cases do you expect to find xanthochromia in lumbar puncture?
- Herpes simplex virus (HSV) encephalitis
- Subarachnoid hemorrhage (SAH)
Prophylactic therapy for cluster headache
- Verapamil
- Alternatives: lithium, valproic acid, topiramate.
Treatment for Pseudotumor cerebri
- Weight loss (obesity main risk factor)
- Acetazolamide➡⬇production of CSF
- Frequent lumbar punctures
- Ventriculoperitoneal shunt if needed
EEG pattern of absence epilepsy (petit mal seizures)
3-per second spike-and-wave discharges
How do you differentiate CSF of SAH vs meningitis when finding elevated WBC?
- SAH➡⬆WBCs (can mimic meningitis), normal WBC:RBC ratio
- Meningitis➡⬆WBCs, ⬆WBC:RBC ratio
*Normal ratio: One WBC for every 500 to 1,000 RBCs (0,002 to 0,001)
Which drugs are associated with the possibility of retarding the progression of Parkinson’s disease?
MAO inhibitors (Selegiline, Rasagiline)
Treatment for Huntington’s disease
No cure or treatment for disease progression. Treat symptoms.
- Dyskinesia: Tetrabenazine, Reserpine
- Psychosis: Atypical antipsychotics (⬇risk for extrapyramidal side effects or tardive dyskinesia)
- Depression: SSRIs
Best first treatment choice for prevention of multiple sclerosis relapse
Glatiramer (copolymer 1) and Beta-Interferon
Which chronic suppressive medication is most likely to cause worsening neurologic deficits in multiple sclerosis?
Natalizumab➡inhibitor of alpha-4 integrin
*Associated with progressive multifocal leukoencephalopathy (PML)
Which is the diagnostic test for Amyotrophic lateral sclerosis?
Electromyography➡widespread denervation and spontaneous action potentials (fibrillation potentials)
What treatments may prevent the progression of Amyotrophic lateral sclerosis?
- Riluzole➡⬇glutamate buildup in neurons
- Edaravone (antioxidant)
Most common complication of Facial nerve palsy. How do you avoid it?
- Corneal ulceration by difficulty in closing the eye (especially at night)
- Taping the eye shut and using lubricants
What do you expect to find in the CSF of Guillain-Barré syndrome?
⬆Protein and normal cell count
What is the most urgent step when you suspect Guillain-Barré syndrome?
Pulmonary function tests➡Assess for ⬇Forced vital capacity and peak inspiratory pressure➡earliest way to detect impending respiratory failure
Best initial test for Myasthenia Gravis
Acetylcholine receptor antibodies (80%-90% sensitive, highly specific also)
Which imaging test should you do in patients with Myasthenia Gravis?
Chest x-ray, CT or MRI (Best CT with contrast)➡look for thymoma or thymic hyperplasia
Best initial treatment for Myasthenia Gravis
Neostigmine or Pyridostigmine➡long-acting cholinesterase inhibitor
*Consider Immunotherapy if remain symptomatic: Corticosteroids, Azathioprine
How may you treat the adverse effects of initial myasthenia gravis therapy?
Glycopyrrolate➡anticholinergic❌muscarinic receptor▶⬇drooling and diarrhea from neostigmine or pyridostigmine
*It does not block nicotinic receptor
Treatment of severe hyperacute crisis of myasthenia gravis
Profound weakness or respiratory involvement➡IVIG or plasmapheresis
How do you differentiate Lambert-Eaton Myasthenic Syndrome (LEMS) vs Myasthenia Gravis?
Increased strength with increased use
*Deep tendon reflexes increase after exercise
Clinical presentation of bupivacaine (local anesthetic) systemic toxicity
- Blocks inhibitory neural pathways➡CNS overactivity▶perioral numbness, metallic taste, tinnitus▶▶generalized tonic-clonic seizures
- Cardiovascular sympathetic activation (tachycardia, hypertension)▶fulminant cardiovascular collapse
In which context may you find bupivacaine (local anesthetic) systemic toxicity?
Epidural anesthesia during labor➡epidural catheter may be inadvertently inserted into maternal circulation➡rapid systemic drug absorption
What is the difference between heat exhaustion vs exertional heat stroke?
Exertional heat stroke has CNS dysfunction, heat exhaustion not
How may you distinguish the cause of recurrent falls?
Pull test
- Abnormal when a patient requires multiple (≥3) steps backward to regain their balance➡impaired postural reflexes
*Early onset postural instability▶Parkinson-plus syndrome (multiple system atrophy, progressive supranuclear palsy, dementia with Lewy bodies)➡postural reflex dysfunction is typically a late finding (>3 years) in Parkinson’s disease
