Nervous System Disorders Flashcards
Pathophysiology of isoniazid toxicity
Overdose causes pyridoxine (vit B6) and GABA deficiency
Clinical scenario of isoniazid toxicity
Seizures usually start 30-120 minutes after severe isoniazid ingestion
Less severe ingestions present as AMS
Tx for isoniazid toxicity
Pyridoxine and benzos (seizures), though pyridoxine only thing that will stop seizures
What are the adverse effects of isoniazid ingestion?
Hepatotoxicity and peripheral neuropathy
Altered mental status, status epilepticus
What are Brudzinski’s and Kernig’s signs?
Brudzinski - Flexing neck causes hips and knees to flex
Kernig - Resistance and pain with knee extension while hip is flexed at 90 degrees
Brudzinski’s - bend the brain; Kernig’s - extend the knees
Cause of normal-pressure hydrocephalus
Most often a build up of CSF due to decreased absorption
Don’t forget to perform this type of exam when working up Bell’s Palsy
Ear exam - otitis media, malignant otitis, mastoiditis can all affect CN VII and look for vesicles that could represent Ramsay Hunt syndrome (Zoster)
Isoniazid is a known cause of what systemic autoimmune disorder?
Systemic lupus erythematosus
Tx for dystonic reaction
Diphenhydramine or benztropine
Cause of extrapyramidal symptoms
Blockade of dopamine receptor leads to a relative acetylcholine excess - hence anticholinergics as tx
Types of extrapyramidal symptoms and time of onset
- Acute dystonia (spasm of tongue, neck, face, and back); hours to days
- Akathisia (compulsive, repetitive motions, agitation); hours to days
- Parkinsonism (tremor, shuffling gait, drooling, stooped posture, instability); 5-30 days
- Tardive dyskinesia (lip smacking, worm-like tongue movements, “fly-catching”); months to years
What is dyschromatopsia?
Change in color perception. Can be a symptom of MS
What will LP show in MS?
50% of cases will show pleocytosis with increased number of lymphocytes.
85-95% of cases will show oligoclonal bands of IgG
Treatment for MS
- Acute attacks: glucocorticoids
- Plasma exchange
- Disease-modifying therapy
- Possibly hematopoietic stem cell transplantation
Hallmark of encephalitis
Abnormal brain function
- AMS
- Psychiatric symptoms
- Emotional lability
- Ataxia
- Seizures
- Lethargy/Coma
- Sometimes focal neuro changes
Most common viral cause of encephalitis
Enterovirus
Anti-N-methyl-D-aspirate receptor autoimmune encephalitis can be the presenting symptom of what tumor?
Ovarian teratoma
Clinical manifestations of optic neuritis
- Sudden loss of monocular partial or complete vision
- Pain with movement of affected eye
- Optic disk pallor may be seen
- Afferent pupillary defect
- Uhthoff phenomenon - transient worsening of vision with increased body temp
Etiologies of optic neuritis
- MS (most common)
- Infection (lyme, herpes, syphilis)
- Autoimmune (lupus, neurosarcoidosis)
- Methanol poisoning
- B12 deficiency
- Diabetes
Tx for optic neuritis
Corticosteroids (IV)
Most common complication with VP shunts
Obstruction - proximal are more common in the first year after placement and 2/2 catheter migration, clot or choroid plexus within the tubing, or tissue debris.
Distal more common 2+ years after placement and include pseudocyst formation in abdomen and disconnection or kinking of the tubing
Infection is second most common
Describe slit ventricle syndrome
Q165329
Where is the most common location for a shunt fracture to occur?
Just above the clavicle
Peripheral vs. Central vertigo
Q312352 table
Clinical presentation of botulism
Descending, symmetric, flaccid paralysis (upper>lower)
- first cranial nerve dysfunction with diplopia, dysphonia, dysphagia, and dysarthria; vertigo also common; decreased salivation -> painful tongue and sore throat
- weakness in upper and lower extremities and muscles of respiration -> tachypnea and respiratory failure
- DTRs may be decreased
- Normal sensory exam
Nonspecific flu-like illness Postural hypotension Parasympathetic blockade - decreased salivation - GI ileus - Urinary retention
Clinical presentation of botulism (infants)
- Constipation
- Weak suck, feeble cry, poor gag reflex, pooled secretions
- Generalized weakness, hypotonia, loss of head control
- “Floppy baby”
Causes of botulism
- Infant: ingestion of honey or corn syrup contaminated with spores
- Food-borne - inadequately preserved or undercooked foods; home canning; ingestion of preformed toxin
- Wound: iatrogenic or inadvertent from cosmetic or therapeutic injection
Management of botulism
- Contact CDC
- Supportive care
- Respiratory monitoring
- Equine serum heptavalent botulism antitoxin (>1 year old)
- Human-derived botulism immune globulin (<1 year old)
- Abx (for wounds)
What is the role of dexamethasone in a child presenting with a high-risk for H. Flu meningitis?
Has been shown to decrease hearing loss associated with H. Flu meningitis in children
Exclusion criteria for tPA
- Significant head trauma or prior stroke in previous 3 months
- Sx suggest SAH
- Arterial puncture at noncompressible site in previous 7 days
- History of prior ICH
- Intracranial neoplasm, AVM, or aneurysm
- Recent intracranial or intraspinal surgery
- SBP >185 or DBP >110
- Active internal bleeding
- Acute bleeding diathesis
- Plt <100,000
- Heparin received within 48 hrs resulting in abnormally elevated aPTT
- Current use of anticoagulant with INR >1.7 or PT > 15 sec
- Current use of direct thrombin inhibitors or direct factor Xa inhibitors with elevated aPTT, INR, or factor Xa assay
- Glucose <50
- CT shows multilobar infarction
- Suspected/confirmed endocarditis
Relative exclusion criteria
- pregnancy
- Sz at onset with postictal residual neuro impairments
- Major surgery or serious trauma within previous 14 days
- Recent GI or urinary tract hemorrhage (within previous 21 days)
- Recent MI (within previous 3 months)
What is the rate of intracranial hemorrhage in patients given tPA for acute myocardial infarction?
Less than 1%
Presentation of carotid artery dissection
- Severe neck, facial, or retroorbital pain
- Unilateral headache
- Pulsatile tinnitus
- Partial Horner (ptosis, miosis)
- Contralateral hemiparesis
Tx for carotid artery dissection
If signs of acute ischemic stroke -> thrombolytic therapy
If no evidence of acute ischemic stroke -> anticoagulation or antiplatelet medication
Remember to start what oral therapy if diagnose SAH
Nimodipine 60mg q4 hrs, ideally given within 4 days of aneurysmal rupture
When is TXA indicated to prevent earlier re-bleeding in patients with aneurysmal SAH?
For short period of time when surgical clipping or endovascular coiling of the aneurysm will be delayed and there are no contraindications to its use
What clinical feature can differentiate a patient with cluster headache from another primary headache syndrome?
Restlessness or pacing behavior
Which medication is recommended as initial preventive therapy for patients with chronic cluster headaches?
Verapamil