Module 9: Neurological Disorders

consciousness

• the state of awareness of self and the environment, and being able to irent to new stimuli

• two components: arousal (wakefulness), content and cognition

arousal (wakefulness)

• maintained by reticular activating system (RAS) involves: brainstem, thalamus, functioning cerebral cortex

• loss of arousal indicates injury to RAS or both cerebral hemispheres

content and cognition

• all cognitive functions (awareness of self, environment, moods, reasoning, judgement)

• involved in awareness:

• selective attention', memory, executive attention

selective attention

ability to select specific information to be processed

memory

ability to store and retrieve information

executive attention

• ability to maintain sustained attention, remember instructions, possess self-control, etc

level of consciousness

can range from:

• coma, stupor, obtundation, delirium, confusion

• assessed by the glasgow coma scale

  • numbered scores are given to responses of eye opening verbal responses and motor responses. total score is an indication of LOC

coma

completely not arousable

stupor

arousable only to pain

obtundation

lower level of arousal, sleepy

delirium

restlessness, hallucinations, delusions

confusion

disorientation, fuzzy thinking, poor response to current stimuli

brain death

• no recovery possible

• determined by:

  • well established underlying pathology

  • deep unresponsive coma and absence of motor reflexes

  • absent brainstem reflexes

  • requires mechanical ventilation - “apnea test”

  • lack of other causes eg. drugs, shock

cerebral death

• irreversible coma

• brainstem may continue to maintain homeostasis, but the individual will never be able to respond in any significant way to the environment

persistent vegetative state

• complete unawareness of self or surrounding enviroment

• persistent sleep wake cycles, brain stem reflexes are intact, but bowel and bladder incontinence(loss of bladder control)

minimally conscious state

• individuals may follow simple commands, manipulate objects, gesture have intelligible speech occasionally

• may enter this state after a persistent vegetative state

locked in syndrome

• complete paralysis of voluntary muscles with the exception of eye movement

• individual is fully conscious with intact, cognitive function, but cannot communicate through speech or body movements

high brain injury

• can result in Cheyne-Stokes breathing: alternating periods of apnea and tachypnea

  • due to response to levels of carbon dioxide in blood

Injury to midbrain

• neurogenic hyperventilation: > 40 breaths per minute when inspiratory/expiratory centres are continuously stimulated

oculocephalic reflex

• movement opposite from head movement (doll’s eye response)

• abnormal = following head movement, or independent movement (assessable only in comatose patients)

decorticate posture

• upper extremities flexed at the elbows and held close to the body and lower extremities that are internally rotated and extended

• may occur with severe cerebral hemisphere damage

decerebrate posture

• increased tone in extensor muscles and trunk muscles, with clenched jaw and extended neck = head in neutral position, all four limbs rigidly extended

• occurs with brainstem lesions

seizure disorders

a sudden, explosive, disorderly discharge of cerebral neurons, that produces a temporary change in brain function, usually involving motor, sensory, autonomic or psychic clinical manifestations and a temporary, altered level of arousal

causes: cerebral lesions, biochemical disorders, cerebral trauma or epilepsy

focal seizure

begin one side of brain

generalized seizures

involves both sides of brain

mild seizures

may manifest as staring spells, no body shaking and may go unnoticed

major seizures

usually produce convulsions

convulsions

jerky, muscle contraction/relaxation cycles

data processing deficits

problems recognizing and processing sensory information

• agnosia, hemineglect, dyspashia, apashia

agnosia

failure to recognize the form/nature of objects; usually only affects one sense

hemineglect

inability to attend to and react to stimuli coming from the contralateral side in space

• wont visually track, orient, or reach to the neglected side. may not use those limbs or take care of them

dysphasia

understanding and use of symbols is disturbed or lost

aphasia

inability to communicate

• wernicke’s, broca’s

wernicke’s aphasia

result of damage to the brain area responsible for the comprehension of language

broca’s aphasia

result of damage to the brain area responsible for the production of language

increased intracranial pressure

• may result from anything that takes up volume in the brain

  • tumour, edema, excess CSF or hemorrhage

• to adjust for increased pressure, there must be a reduction. in some other cranial content: blood volume, CSF volume, tissue volume → monro-kellie hypothesis

• loss of CSF

• cerebral blood volume and flow

cerebral edema

• increase in the fluid content, causing increase in brain tissue volume

• occurs after trauma, infection, hemorrhage, tumour, ischemia, infarct or hypoxia

• distorts blood vessels

• vasogenic & cytotoxic

vasogenic edema

increased permeability of blood-brain-barrier : plasma proteins leak out of capillaries → increased water content of tissue

• occurs mainly in white matter

cytotoxic edema

• toxins or hypoxia cause failure of transport mechanisms of cells → more sodium inside cell → more water inside cell

• occurs mainly in grey matter

hydrocephalus

• excess fluid in ventricles

• caused by excessive CSF production or too little reabsorption

noncommunicating (obstructive)

obstruction prevents CSF from reaching arachnoid villi and being reabsorbed

communicating

failure of reabsorption due to reduced number or scarring of arachnoid villi (due to meningitis)

• overproduction of CSF caused by adenomas of choroid plexus (much rarer)

alterations in muscle tone

muscle tone: normal state of muscle tension allowing for controlled movement and maintenance of posture; controlled by the stretch reflex

causes: injury to any section of motor pathway- peripheral nerve, neuromuscular junction, spinal cord, brain

symptoms: hypertonia, hypotonia

hypertonia

• rigidity : injury to upper motor neurons produces increased tone

hypotonia

• flaccidity

• injury to the LMN, produces decreased tone

paresis

weakness

paralysis

loss of motor neuron function so that a muscle group is unable to overcome gravity

hyperkinesia

• excessive movements

• due to physical or chemical causes

basal ganglion posture

• stooped, hyperflexed with narrow, short-stepped gait

spastic gait

a shuffling gait with leg extended and held stiff

scissor gait

stiff legs that swing around and cross infront

hypermimesis

inappropriate laughter or crying

dyspraxia/apraxia

inability performing tasks that require learned motor skills

problem is with use of muscles

dysarthria

• inability in speaking

agraphia

inability in writing

focal brain injury

specific, grossly observable brain lesions that occur in a precise location

contusion

bruise in brain tissue

blood leaking from injured vessels

effects peak 18-36 hours after injury

coup injury

impact against an object, causing direct trauma to brain at point of impact

contrecoup injury

from rebound of brain against opposite side of skull, causing impact injury at brain area opposite to object, and sheering forces through brain

hematoma

bleeding in/beside the brain as a result of trauma can produce an area filled with blood

extradural (epidural) hematoma

• injury (usually a fracture) causes bleeding between the dura mater and the skull, predominantly due to arterial bleeding

• lucid period 2-3 hrs b/w injury and clinical signs → rapid deterioration

subdural hematoma

• venous, low pressure, slow bleeding

intracerebral hematoma

• bleeding within the brain

• penetrating injury or sheering forces traumatize small blood vessels

• may be delayed, 3-10 days after injury

• signs and symptoms depend upon location in the brain

diffuse brain injury

• diffuse and widespread damage to neural axons in the brain

• result of shaking, rotational and twisting movements

• can be observed only with microscope

• least severe form → concussion

classic cerebral concussion

loss of consciousness for up to 6 hr

confused state lasts for several hours, headache, nausea, retrograde amnesia

mild DAI

(6-24hr coma) may display decerebrate or decorticate posturing with extended periods of stupor/restlessness

moderate DAI

(>24hr coma) may display above posturing with unconsciousness lasting days or weeks. on awakening , often permanent deficit in memory, reasoning, language, etc

severe DAI

(usually emerge from coma in the first 3 months after injury), however, initial injury eventually results in compromised coordinated movements, verbal and written communication skills, inability to learn and reason

secondary brain trauma

• indirect result of primary trauma

• mechanisms include cerebral edema, IICP, decreased cerebral perfusion pressure, ischemia and brain herniation

• damage hours to days after primary trauma

cerebrovascular disease

any abnormality of the brain caused by pathologic process in the blood vessel

result: ischemia, or hemorrhage

stroke

acute focal neurological deficit from a vascular disorder that injures brain tissue

thrombotic stroke

• ischemic stroke

• large vessel

• occlusions formed by thrombi developping in large arteries within the brain

• causes acute ischemia

• affects cerebral cortex

  • symptoms: aphasia, neglect, visual field defects

• seen in older

• not associated with activity, may occur at rest

lacunar stroke

• ischemic stroke

• small vessel

• very small infarctions deep in the brain

• can be due to emboli, small hemorrhages, vasospasms

• internal capsule, basal ganglia, brainstem → effects are different than large vessel strokes

  • more sensory/motor based effects

• at risk: chronic hypertension, diabetes

embolic stroke

• ischemic stroke

• fragments that break from a thrombus formed outside the brain (thrombus usually within the left heart, but could be within carotid artery)

• middle cerebral artery

• sudden onset with immediate maximum defecit

• causes: rheumatic heart disease, atrial fibrillation, recent heart attack

transient ischemic attack

• ischemic stroke

• brief episode of neurologic dysfunction caused by a focal disturbance of brain with symptoms lasting less than 1 hr, with no evidence of infarction and complete clinical recovery

• manifestations numbness in face, arm or leg, trouble speaking or understanding, poor vision in one or both eyes, confusion, etc

• result of platelet clumps or vessel narrowing with spasm

• high risk of repeat occurrence and eventual stroke

hemorrhagic stroke

• most fatal stroke

• occurs suddenly, with activity

• rupture of blood vessel, bleeding into tissue, forming a growing mass of blood (hematoma), accompanied by edema

• causes: hypertension, ruptured aneurysms, trauma

• manifestations: vomitting at outset, headache

• great danger = increased intracranial pressure → coma and death

intracranial aneurysm

• 2mm to 2-3cm

• classified on the basis of shape

• asymptomatic

• first indication is acute subarachnoid hemorrhage and/or intracerebral hemorrhagepa

parkinson disease

• most common movement disorder ; affects 1-2% of those >65 yrs

• degeneration of the basal ganglia and loss of dopamine producing cells in substantia nigra and corpus striatum

• three cardinal symptoms

  1. resting tremor

  2. bradykinesia

  3. muscle rigidity

• l-dopa reduces symptoms but produces other motor side effects

alzheimer disease

• most common causes of severe cognitive dysfunction in older persons ; leading cause of dementia

• plaques form between neuron’s, tangles form inside neuron’s, damaging and killing neurons’, disrupting nerve impulse transmission

• no cure