Neurological Disorders (stroke, TBI, seizures, migraines)

Leading cause for stroke

-hypertension (high BP)

(also athlerosclerosis, hardened arteries from plaque build-up)

Ischemic stroke

from blockage in artery

Hemorrhagic stroke

from bleeding in the brain

Thrombotic vs. embolic stroke

thrombotic – ischemic stroke (blockage), from a blood clot in brain

embolic – blood clot formed elsewhere in body and traveled

Transient ischemic stroke

<5min, artery was blocked causing limited oxygen to brain

-medical emergency + warning sign for future strokes

Intracerebral vs. subarachnoid hemorrhagic stroke

Intracerebral hemorrhagic stroke – bleeding d/t artery rupture in brain

Subarachnoid – bleeding in the space btwn brain and membrane covering

Sxs of stroke involving Anterior cerebral artery

Executive (frontal lobes) + legs/feet

-impaired insight and judgment

-apathy, confusion

-mutism, urinary incontinence

Sxs of stroke involving Middle cerebral artery

Face/Arm + Language (L) + Spatial (R)/parietal lobe

-L/language: aphasia

-R/spatial: apraxia, contralateral neglect

-dysarthria (slurred speech)

-MCA is most commonly involved in strokes

Stroke sx of contralateral neglect (which artery?)

Right MCA

Stroke sx of aphasia (which artery?)

Sxs of stroke involving Posterior cerebral artery

Occipital lobe

Photographer: photos (vision) in the past (memory)

-Memory loss

-Visual agnosias

Traumatic brain injury

-can produce loss of consciousness + range of sxs once consciousness is regained (emotional/cognitive/physical sxs, sxs are indefinite)

-most recovery occurs in first 3 months, and 1 yr

Post-traumatic amnesia

-another name for anterograde amnesia post TBI

Cognitive and emotional sxs following TBI

(If Melanie forgot me 😢)

Cognitive: anterograde + retrograde amnesia

-anterograde amnesia duration > retrograde amnesia, duration = predictor of TBI severity, and sx recovery

Emotional: depression, irritability

Aprosodia

-loss of ability to express and understand prosody (tone, pitch, rhythm, volume)

-caused by damage to R hemisphere, which is responsible for emotional prosody and pragmatics (TBI or stroke)

Physical sxs following TBI

-Seizures

-nausea, vomiting, headache

-sleep disturbance

Post-traumatic seizures

-Seizures that occur <1week post-TBI

-Treated with anti-seizure medication

Post-traumatic epilepsy

-Seizures occuring >1 week post-TBI

-Harder to treat

-Txs: vagus nerve stimulation, responsive neurostimulation (for seizures, detects abnormal electrical activity, like pacemaker for brain), surgery

Seizure (what is it?, provoked vs. unprovoked)

-transient abnormal electrical activity in brain, causing physical or behavioral alteration

-provoked = known cause (e.g., TBI, stroke, alcohol withdrawal, central NS infection, fever)

-unprovoked = no known cause

Focal onset vs. generalized onset seizures

Focal onset (aka partial seizures) = only in 1 hemisphere of brain → affects 1 side of body (but can spread)

Generalized onset = originates in both hemispheres

Focal onset aware seizures

-aka simple partial seizures

-focal onset, don’t affect consciousness

Focal onset impaired awareness seizures

-aka complex partial seizures

-focal onset, causes altered consciousness

Temporal lobe seizures (sxs)

-most common focal-onset seizure area

(Limbic system connection)

→ Autonomic sxs: tachycardia, sweating, dilated pupils

→ Sudden intense fear/emotion, déjà vu (familiarity), jamais vu (unfamiliarity); may begin with aura

(Closeness to olfactory/gustatory centers)

→ lip-smacking, repeated chewing/swallowing, fidgeting, picking at clothing, other automatisms

(Wernicke’s area)

→ trouble speaking, impaired comprehension

Frontal lobe seizures (sxs)

“Motor cortex & midnight” seizure

-Motor: repetitive movements (kicking, pedaling, rocking), abnormal posture (fencing posture)

-Midnight: often occur during sleep, <30 seconds

-Broca’s area:

→ trouble speaking, explosive screams and laughter (purely mechanical, vocal motor program triggered)

Parietal lobe seizures (sxs)

“Body image” seizure, d/t somatosensory cortex

-body image distortions; body part feels enlarged/shrunken/absent;

-abnormal sensations: tingling, numbness, pain

-feelings of movement (e.g., floating)

Occipital lobe seizures (sxs)

“Visual light show” seizure

-rapid blinking, fluttering

-bright lights, flashing lights (simple visual hallucinations)

-partial blindness, impaired visual acuity (blurriness)

Two types of generalized onset seizures

-motor seizures, aka tonic-clonic (or grand mal)

-non-motor seizures, aka absence (or petit mal)

Generalized onset motor seizures

(Tonic-clonic/grand mal)

-altered consciousness

-tonic phase: stiffened muscle tone in upper body (face, limbs)

-clonic phase: rhythmic jerking in arms/legs

-once consciousness is regained → depression, confusion, fatigue, no memory of events during seizure

Generalized onset non-motor seizures (absence/petit mal)

-blank stare, rapid blinking

-very brief (5-15 sec) sudden loss of awareness

Status Epilepticus

(status of epilepsy)

-prolonged seizure activity:

-single seizure (≥5 min)

-or, multiple seizures w/o returning to consciousness in btwn

Generalized convulsive status epilepticus

Convulsive = tonic-clonic/motor seizures

-tonic-clonic seizures >5 min, w/ loss of consciousness

-life-threatening emergency

Non-convulsive status epilepticus

-No prominent motor sxs

-May have altered consciousness, and other seizure sxs (e.g., automatisms, aphasia, delusions/hallucinations)

Status epilepticus ←→ neurotransmitter abnormalities

(GABA + glutamate)

-early stages of SE: GABAnergic inhibition fails, especially in hippocampus

-during established SE: glutamate excitation further potentiates the seizure, leading to prolonged seizure that spreads from hippocampus to neocortex

What are some causes of status epilepticus?

-TBI, stroke, central NS infection

-autoimmune disorders

-drug toxicity

-non-compliance with seizure meds

Treatment of status epilepticus

(Increase inhibitory GABA)

-first-line = benzos

-anti-seizure medications, when benzos are ineffective, and for maintenance/prevention

Migraine headaches

-Low serotonin

-Abnormalities in glutamate, dopamine, and norepinephrine (all but ACh, GABA)

-neurovascular event: electrical activity triggers nerve → dilation of blood vessels

Preventive medications for migraine headaches

migraines = neurovascular events, linked to low serotonin

-antidepressants (serotonin)

-beta blockers (vascular, stabilizes blood vessel widening/constricting)

-anti-epileptics (neuro)

Acute (abortive) medications for migraine headaches

-Anti-inflammatories (NSAIDs, acetaminophen)

-Triptans (serotonin agonists: think triptophan/serotonin)

Primary hypertension

-”silent killer,” 90% of hypertension cases

-high BP with NO known cause

(secondary hypertension = high BP d/t a known disease)