Neurological Disorders

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

-Left: aphasia

-R: 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

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

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)

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

-Connection to limbic system

→ 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, but intact comprehension

→ vocal motor program triggered: explosive screams and laughter (purely mechanical)

Parietal lobe seizures (sxs)

“Body image” seizure, d/t somatosensory cortex

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

-tingling, numbness, pain, and other abnormal sensations

-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

-prolonged seizure activity:

-single seizure (≥5 min)

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

Generalized convulsive status epilepticus

(Convulsive, motor sxs)

-tonic-clonic seizures, w/ loss of consciousness

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 activity

-failure in GABA (inhibitory) + glutamate (excitatory) potentiation

-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

-first-line = benzodiazepenes

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