Treatment of Epilepsy

Anticonvulsants

Dilantin (phenytoin)

Tegretol (carbamazepine)

Depakene (valproic acid)

Depakote (divalproex)

phenobarbital

Valium (Diazepam)

Ativan (lorazepam)

Clonopin (clonazepam)

Neurontin (gabapentin

Mysoline (primidone)

Zarontin (ethosuximide)

Good control achieved in about 75%

(anticonvulsants are also used for other purposes)

Treatment Alternatives

Surgical removal of epileptic focus

Select cases may benefit from strict high fat ("ketogenic) diets to alter brain chemistry

Avoid possible triggers (stress, fatigue, flashing lights, alcohol, excess caffeine, fever, hyperventilation, hypoglycemia)

Frontal Lobes (~1/3 of cortex)

Motor control

Higher cognitive or executive functions

Self-regulation (behavioral inhibition, sensitivity to social cues, conscience)

Initiative

Anatomy

The frontal lobe is heavily interconnected with:

basal ganglia & other components of the motor system

all other lobes of cortex

limbic system

Beyond Motor Planning

Frontal lobe has evolved from being the main motor planner/organizer to a higher level behavioral/strategic planner/organizer.

Provides us with a mental model, considering options, selecting behaviors based on context, feedback, stored knowledge; adapting to the situation

What are executive functions?

Forming goals, considering consequences

Considering response alternatives

Choosing / initiating goal-directed behaviors

Self-monitoring your responses

Correcting/modifying behavior as necessary

Persistence despite distraction

Causes of Frontal Damage

traumatic brain injury

neoplasms (tumors)

vascular lesions (stroke)

degenerative diseases that affect frontal pathways (Alzheimer’s, Parkinson’s, Huntington’s, Pick’s disease, Lewy body disease) and cause dementia

Effects of Frontal Damage

Decreased consideration of alternative strategies/behaviors; reduced flexibility

Decreased spontaneity, initiative, may appear lazy, unmotivated

Knowledge/intelligence may seem intact (e.g. IQ) but its not used to generate strategies or solve problems efficiently

Decreased Inhibition

Problems inhibiting incorrect/ineffective responses & switching to a new strategy

Perseverates; not responsive to feedback or changes in environment

Violates rules, expectancies; takes risks

Emotionally reactive

Decreased social inhibitions as well; disinhibited personality; impulsive

Decreased Temporal Memory

Impaired memory for order, recency, contextual info

Could affect problem-solving, planning and impair systematic, organized behaviors

Possible Personality and Emotional Changes

Lack of tact & restraint, immature, coarse,lack of social graces, inappropriate sexual behavior, increased motor activity. More common after orbitofrontal or right frontal damage; called "pseudopsychopathic"

Another Possible Personality Change

Apathetic, indifferent, loss of initiative, lack of emotion or somewhat depressed, little verbal output ("apathetic-akinetic mutism). Most common after cingulate damage or left frontal damage; called "pseudodepression"

Some Neuropsych Tests Used

Wisconsin Card Sorting Test; Stoop Test

Word Fluency Test; Design Fluency Test

Visual Search Test

Motor stength, speed and sequencing

test for aphasia, anosmia

The Parietal Lobe Regions

Primary and secondary somatosensory cortex

Multimodal association cortex

Luria’s View of Sensory Processing Deficits

Primary sensory cortex damaged: Impairment of basic sensory awareness

Secondary sensory cortex damaged: Agnosia (modality-specific impairment of recognition of what is sensed.

Tertiary (association) cortex damaged: Deficits in integrating that sensory input with other modalities, memory, language, etc.; difficulties using/applying sensory information

Lateralization of Parietal Functions

Left parietal: sensory & integrative processing important for normal language and math

Right parietal: sensory & integrative processing related to the use of spatial information in perceptual, cognitive & motor behaviors

Left Parietal Damage

Anomia: not able to name things

Alexia: not able to read

Agraphia: not able to write

Acalculia: loss of math abilities

Impaired grammar

Impaired left/right discrimination

Right Parietal Damage

Contralateral sensory neglect

"Constructional" apraxia-can’t assemble, build, draw, construct because of visuomotor/spatial impairment

Dressing apraxia (other ideomotor apraxias - left parietal)

Poor map reading/drawing

Impaired ability to recognize unfamiliar views of objects

Tests For Parietal Function

2 point discrimination (tactile sensation)

Seguin-Goddard Form Board (tactile recognition)

Golin Incomplete Figures; Mooney Closure Test (complex visual perception)

Semmes test of extrapersonal orientation

Kimura box test (motor learning)

Temporal Lobe Regions

Auditory area - superior temporal gyrus (primary & secondary auditory cortex)

Complex association cortex - middle & inferior temporal gyri (links audition-vision-memory system)

Limbic region - medial temporal cortex (personality?) & amygdala (emotion) & hippocampus (memory storage process)

Effects of Temporal Damage

Auditory impairment; word deafness; Wernicke’s aphasia

Visual agnosias; prosopoagnosia; impaired selective attention

Impaired storage of new memories; possible loss of long-term memories

Emotional & personality changes

Limbic Memory Regions

Essential for the storage of new memories

hippocampus

mammillary bodies and medial thalamus

Remembering emotional aspects

amygdala

Areas affected by Alzheimer’s disease

hippocampus and surrounding cortex, amygdala, nucleus basalis of Meynert

Temporal Lobe Epilepsy

Complex partial epilepsy (psychomotor)

Typically epilepsy is not associated with mental illness, but TLE is (~45% vs 10% have psychiatric symptoms, changes in affect & personality. Other types of temporal lobe pathology may also affect these aspects of behavior.

Emotional & visceral aura; rubbing and oral movements; hallucinations & disordered thought

Temporal Lobe Personality

Data on TLP is not consistent but these are some of the qualities that may be associated with TL abnormalities:

humorlessness; paranoia; feel threatened

overemphasis on details/minutiae; verbose

egocentric, "sticky" personality, sense of destiny

religiosity, focus on good vs evil

aggressive outbursts (temporal lobe pathology has been found in brains of several mass murderers and has been used as a defense by others)

Limbic System & Aggression

Abnormalities in hypothalamus or amygdala can also cause outbursts of rage or violence.

Rage in rabies associated with viral infection of hippocampus/amygdala

Amygdalectomy is a psychosurgery that has been used to treat episodic dyscontrol (attacks of rage)

Broca’s Aphasia

damage to frontal lobe language area

patient not articulate, not fluent

speech slow, difficult, & much reduced

comprehension relatively intact, but

comprehension of grammatical words, devices, and endings is impaired

production of sign impaired in the deaf

Wernicke’s Aphasia

temporal lobe language area damaged

speech is fluent, but nonsensical

reduced comprehension of language

confusion of phonemes

comprehension of sign language ok

Dyslexia

less lateralization

more likely to be bilateral or reversed

often small brain abnormalities

altered visual attention/perception

Williams Syndrome

excellent language abilities

impaired visual/spatial abilities

low overall IQ, less cortical development

Blood Supply to the Brain

2 Internal carotid arteries on either side of the neck

2 Vertebral arteries on either side of the spinal column, join to form a single basilar artery on anterior surface of brainstem

All interconnected at the "circle of Willis"

Stroke or Cerebrovascular Accident

Death or damage of some portion of the CNS due to disruption of normal blood supply to that area

Area of damaged/dead cells is called the infarct.

500,000/year in US

2 Main Varieties

ischemic stroke - obstruction of artery deprives the tissue beyond that point of its supply of oxygen & energy ("ischemia" refers to a localized decrease in blood supply)

hemorrhagic stroke - artery ruptures causing both intracerebral bleeding & failure to supply blood to tissues beyond that point

Common Treatable Risk Factors

Hypertension (high blood pressure)

Cigarette smoking; alcohol abuse

Hyperlipidemia (high fats & cholesterol)

Heart disease

Diabetes

Symptoms of Stroke

Depend on particular blood vessel affected and the site and extent of brain damage

Large Vessel Stroke

Blockade of a major artery by an embolus (a traveling clot or bit of matter carried by bloodstream until it lodges in a vessel too small for it to pass thru. If a person suffered a stroke due to a lodged embolus, we would say they had suffered an "embolism".)

Common sources of emboli

Heart problems (atrial fibrillation, enlarged heart, heart valve problems, damage due to heart attack)

Atheroma (fatty deposits in arteries)

Large Vessel Stroke

Blockade of a major artery by a thrombus (a clot that forms within an artery - usually because of atherosclerosis

Aspirin or other anticoagulant therapy can lessen the risk of clots

Small Vessel Stroke

Occlusion of small vessels produces a smaller area of ischemia and infarction

Small infarct are often called "lacunae"

Common locations: internal capsule, basal ganglia, thalamus, pons.

Really small lacunar strokes may go un-noticed.

Hemorrhagic Stroke

Intracerebral hemorrhage in basal ganglia, thalamus, pons, or cerebellum related to hypertension, smoking, alcohol, cholesterol, stimulant abuse or anticoagulants.

Causes stroke symptoms + risk of increased intracranial pressure & herniation due to hematoma.

Subarachnoid Hemorrhage

SAH may be due to head injury

primary SAH due to ruptured aneurysm

Symptoms: sudden severe headache, nausea & vomiting, fainting

Headache, pain behind eyes & stiff neck may precede SAH

Risks - rebleeding, hydrocephalus, ischemia from vasospasm

CT scan or spinal tap to show blood

Other Stroke Terms

Transient Ischemic attack - short-term disruption of blood supply to region with reversal of symptoms within minutes to hours.

Reversible ischemic neurologic deficit (RIND)- resolves within 24 hrs.

Stroke in progress or in evolution - increasing symptoms of stroke