Neurological Emergencies Flashcards
Causes of SAH:
*80% of non-traumatic hemorrhages from ruptured saccular aneurysms (At points where go to smaller vessels, change in level of turbulence.)
*Other causes: AV malformations, neoplasms, blood dyscrasias (pre-disposed to bleeding complications)
Classic presentation of SAH:
*“thunderclap” onset
*10-25% will have a seizure
*Often within minutes of onset
*Neck stiffness, photophobia, Low back pain
*Sounds like meningitis but with meningitis CANNOT move at all due to pain and would have a fever
*Sudden onset of worst headache of life.
*Worse on exertion eg valsalva, exercise.
*75% of patients have nausea and vomiting.
How can R/O menigitis without labs?
*The absence of fever, neck stiffness and altered mental status in a patient with a headache virtually eliminates the diagnosis of meningitis.
What is pseudotumor cerebri?
*Condition (or group of conditions) characterized by the presence of elevated intracranial pressure (>20 cm H20) with no obvious underlying cause
AKA:
*Idiopathic Intracranial Hypertension
*Benign Intracranial Hypertension
Almost all afflicted patients have papilledema→ Optic disc/nerve atrophy can result in significant and permanent visual loss, even blindness
Classic presentation of pseudotumor cerebri:
*Obese female of child-bearing age
*Headache is:
*Retro-ocular, pulsatile headache
*HA is worsened by any maneuver that increases ICP
*Valsalva, squat, etc.
*Other “classic” presenting symptoms:
*Nausea 30%
*Visual loss 30-60%
*Double vision 30%
order of vision loss with pseudotumor cerebri (if occurs):
*Early changes include loss of peripheral fields and loss of color vision
*Central vision is affected later
Tx for pseudotumor cerebri:
*Visual loss but no headache:
→Optic Nerve Sheath Fenestration if vision deteriorates
*Medical management
→Pain meds for headache/subjective complaints
→Carbonic anhydrase inhibitors to decrease CSF production
→Lasix, steroids, etc.
*Intervention (for those refractory to medical management)
→Serial Lumbar Punctures
→Shunt placement (Lumbar/Ventriculo-peritoneal)
pathogenesis of cerebral venous thrombosis:
Brain dumps veins into sinuses rather than capillary beds
Big, slow moving veins tend to clot→risk of H/A and if persists, infarction (almost stroke like) or drives the pressure up
*A prothrombotic risk factor is identified in about 85% of cases
*Favors a 2-hit model
*Oral contraceptives
*Particularly 3rd generation
*Accounts for up to 75% of all cases
What is one common cause of stroke in the young (slight male predominance)?
*Traditional stroke risk factors not shown to be statistically significant
Cerebral Artery Dissection: in <45 years, accounting for 8-25% of strokes
What is Physiologic Vertigo?
“motion sickness”
*Mismatch between visual, proprioceptive and vestibular inputs
*Not a diseased cochleovestibular system or CNS
What is Nystagmus?
Rhythmic slow and fast eye movement
*Direction named by fast component
*Slow component due to vestibular or brainstem activity
*Slow component usually ipsilateral to diseased structure
*Fast component due to cortical correction
What are two broad categories of vertigo?
Periph (inner ear)
vs
Central (inside head—stroke cerebellar infarct)
characteristics of inner-ear causes of vertigo:
- Onset: Sudden
- Severity of Vertigo: Intense
- Pattern: Paroxysmal
- Exac. by movement: Yes
- Autonomic: Frequent
- Laterality: Unilateral
- Nystagmus: Horizontorotary
- Fatigable/Fixation: Yes (diminishes with repeat testing)
- Auditory symptoms: Yes
- TM: May be abnormal
- CNS symptoms: Absent
Findings with CNS-derived (central) vertigo:
Onset: Usually slow
Severity of Vertigo: Usually mild
Pattern: Constant
Nystagmus: Any
Fatigable/Fixation: No
Auditory symptoms: No
TM: normal
CNS symptoms: Present
peripheral vertigo DDx:
- Benign paroxysmal positional vertigo (BPPV)- Short-lived episodes brought on by rapid changes in head position
- *Otoconia displacement, No hearing prob
- Labyrinthitis- Middle ear infection of some sort
- Ménière disease- Abrupt/ recurrent episodes, severe rotational vertigo
- Vestibular neuronitis- Sudden onset, increases in intensity over hours and subsides over several days
-
Acoustic Neuroma- Tumor of the Schwann cells around the 8th CN. *Earliest sign is decreased corneal reflex (blink reflex, elicited by stimulation/touching the cornea)
*Later truncal ataxia *Most occur in 30, 60yo women
