chapter 16: disorders of brain function

3 main parts of brain

• cerebrum: divided into 2 hemispheres

• cerebellum: little brain

• brainstem: divided into midbrain, pons, & medulla oblongata

protective structures of brain

• cranial meninges and associated spaces

• carnial bones

brainstem

divided into midbrain, pons, and medulla oblong

cerebral circulation

it delivers oxygen and nutrients for its metabolic needs, and to remove CO2 + other waste products

picture of structural parts of brain

cranial meninges

• dura mater: thick, tough membrane - outermost

• arachnoid mater: lies directly below mater - middle

• pia mater: very thin, delicate membrane covering brain surface - inner

circle of willis

network of brain arteries that provide alternative pathways for blood flow in case of blockage

brain injuries classified into two categories:

focal brain injury & global brain injury

focal brain injury

• caused by localized neurologic deficits

• symptoms correspond to the injured brain region

global brain injury

• affects entire brain

• usually results in altered consciousness

brain injuries manifested by:

• changes in lvl of consciousness

• alterations in cognitive function

• motor dysfunction

• sensory impairment

coup-contrecoup injury

type of injury in which brain damaged at both sites of impact due to rapid movement of brain within skull

coup injury

• occurs directly beneath site where head is struck

• person hit in forehead

• frontal lobe impacts inside of skull at point of impact, contusion develops

contrecoup injury

• occurs on side opposite of impact

• after striking front of skull, brain rebounds backward

• occipital region hits inner surface of skull = second contusion develops on opposite side (occipital lobe)

photo of primary and secondary impact

brain injury occurs when:

brain tissue is damaged by a physical force, loss of blood, lack of oxygen, infection, toxins

mechanism of injury depends on cause; there are two types:

primary brain injury and secondary brain injury

primary brain injury

• immediate damage occurs at time of insult

• ex: head trauma, causing bruising or tearing of brain tissue

mechanism of primary injury

• mechanical disruption of neurons and glial cells

• tearing of axons

• direct injury to blood vessels

secondary brain injury

• develops minutes to days after initial injury and often causes additional damage

• ex: ischemia and hypoxia, excitotoxicity

ischemia and hypoxia (secondary brain injury)

• reduced blood flow or oxygen delivery deprives neurons of oxygen and glucose

  • ATP production fails

  • ion pumps fail, causing cellular swelling + dysfunction

excitotoxicity (secondary brain injury)

• injured neurons release excessive amounts of neurotransmitter glutamate

  • glutamate stimulates NMDA & AMPA receptors

  • excess calcium enters cells

  • result in activation of destructive enzymes, damage to cell membranes, proteins, and DNA

role of glutamate NMDA receptor in brain cell injury:

• glutamate is principal excitatory NT in brain

• prolonged ischemia results in glutamate transporters become immobilized and ineffective, extracellular glutamate accumulates

concussion

temporary disturbance of brain function caused by blow to head, resulting in disruption to delicate axonal fibers + white matter tracts that project cerebral cortex

• no structural brain damage visible on imaging

• temp neurological dysfunction

• may involve brief loss of consciousness or none at all

signs & symptoms of concussion

• headache, dizziness, confusion

• amnesia

• nausea and vomiting

• blurred vision and sensitivity to light or noise

contusion

bruise of brain tissue caused by direct trauma, resulting in structural damage and localized bleeding

• more severe than concussion

• involves hemorrhage, edema, and tissue injury

• often occurs beneath site of impact (coup injury) or opposite side of brain (contrecoup injury)

signs & symptoms of contusion

• signs of increased intracranial pressure

  • altered lvl of consciousness, persistent headache, nausea, and vomiting

• seizures, weakness, or paralysis

hematomas

• result from injury to blood vessels and subsequent bleeding

• blood can accumulate within diff compartments of skull

• classified into four main types:

  • epidural, subdural, intracerebral

epidural hematoma

• collection of blood between inner surface of skull and dura mater (outermost meningeal layer)

• caused by rupture of middle meningeal artery

• manifestations: an initial loss of consciousness, a temporary "lucid interval" of seeming recovery, and a subsequent rapid neurological decline

subdural hematoma

• collection of blood between dura mater and arachnoid mater

• results from tearing of bridging veins that connect cerebral cortex to dural venous sinuses

• venous bleeding occurs more slowly than arterial bleeding seen in epidural hematomas

• manifestations similar to epidural hematoma

intracerebral hematoma

• collection of blood within brain tissue

• results from severe movement of brain during head trauma or progression of cerebral contusion into hematoma

• manifestations: vary depending on size + location of hematoma

picture of locations of hematomas

picture of mechanisms of bleeding in subdural hematoma

reticular activating system (RAS)

• network of neurons located in brainsteam (midbrain, pons, and upper medulla)

• plays role in regulating arousal, alertness, wakefulness, and consciousness

what sensory input does RAS receive and what does it receive

it receives sensory input from visual, auditory, and tactile sensory pathways!

what do these signals from RAS increase?

cortical activity = enabling awareness, attention, and wakefulness

level of consciousness (LOC)

• degree of awareness of self + environment and ability to respond to stimuli

• stimuli: full consciousness, confusion, lethargy, obtundation, stupor, coma (cant be awakened by any stimuli)

lethargy (LOC)

• reduction in mental alertness where person appears drowsy

• very slow in mental processes, motor activity, and speech

• responds appropriately to painful stimuli

obtundation (LOC)

• decreased alertness and interest in environment

• requires repeated verbal stimulation to maintain attention

• responses are slower and less accurate

stupor (LOC)

• can only be aroused by vigorous or painful stimuli

• minimal verbal responses

• returns to unresponsive state when stimulation stops

glasgow coma scale (GCS)

• neurological scoring system used to assess LOC after head injury or in critically ill patients

• components of GCS include:

  • eye opening (E): scores 4-1

  • verbal response (V): scores 5-1

  • motor response (M): scores 6-1

• total score:

  • GCS = E + V + M; ex: 3+4+6=13/15

  • max: 15 (fully alert)

  • min: 3 (deep coma)

abnormal flexion and extension are:

abnormal motor responses assessed in GCS!

decorticate and decerebrate posturing are:

• indicators of severe neurological injury

• postures help localize neurological lesions + assess severity

• as coma progresses, motor tracts are interrupted at specific lvls initiate rigidity + abnormal postures

decorticate posture

• appearance:

  • flexion of arms, wrists, and fingers

  • arms adducted toward body

  • lower extremities internally rotated, feet plantar flexed

• cause:

  • lesions of cerebral hemispheres

  • damage to internal capsule

decerebrate posture

• appearance:

  • arms rigid and extended

  • palms turned away from body

  • legs stiffly extended

  • feet plantar-flexed

• cause:

  • lesions involve diencephalon, midbrain, and upper brainstem

  • associated w/ poorer prognosis than decorticate posturing

brain death

• irreversible loss of function + entire brain, including brain stem

• body cannot maintain internal homeostasis

  • no conscioussness, no brain reflexes (pupils don’t react to light), and no ability to breathe independently

cerebral death

• irreversible loss of function of cerebral hemispheres; brainstem function is present

  • no awareness of higher mental function

  • brainstem may still control breathing, heart rate, and reflexes

intracranial pressure (ICP)

• pressure that opposes blood entry into brain

• total intracranial volume remains constant so normal adult ICP is 5-15 mmHg

ICP reflects balance between

• brain balance (~80%)

• cerebral blood volume (~10%)

• cerebrospinal fluid (~10%)

• increase in one component must be compensated by a decrease in one or both of the others; otherwise ICP rises!

monro-kellie hypothesis

• brain tissue, blood, and CSF volumes reciprocally adjust to maintain a normal ICP

• change in one component is balanced by equal + opposite effect in one or both of remaining components

blood reaches brain only when:

• cerebral perfusion pressure (CPP) is adequate!

• CPP = mean arterial pressure (MAP) - intracranial pressure (ICP)

mean arterial pressure (MAP):

pressure pushing blood into brain

when ICP rises:

• compression of cerebral blood vessels occurs

• CPP decreases

• cerebral blood flow falls

• brain tissues receives less oxygen and glucose

• cerebral ischemia + neuronal injury develop

brain herniation

• displacement of brain tissue from normal position due to increased ICP, causing it to move across rigid intracranial structures such as: falx cerebri, tentorium cerebelli, or foramen magnum

  • life-threatening neurological emergency

  • compression of vital brain structures and blood vessels

common causes of brain herniation

• traumatic brain injury

• intracerebral hemorrhage

• brain tumors

types of brain herniation:

cingulate, uncal, central

cingulate (brain herniation)

• cingulate gyrus is pushed beneath falx cerebri

  • may compress anterior cerebral artery

  • signs: unilateral or bilateral leg weakness

uncal (brain herniation)

• medical temporal lobe (uncus) herniates through tentorial notch

  • compresses ipsilateral third cranial nerve

  • signs: dilated, fixed ipsilateral pupil, decreased consciousness

central (brain herniation)

• downward displacement of diencephalon and brainstem

  • signs: progressive loss of consciousness, decorticate posturing

picture of brain herniation

hydrocephalus

• condition in which excess cerebrospinal fluid accumulates within ventricles of brain

• three types: noncommunicating, communicating, overproduction

noncommunicating (hydrocephalus)

• CSF flow blocked within ventricular system

• ex: aqueductal stenosis, tumors, congenital malformations

communicating (hydrocephalus)

• CSF reaches subarachnoid space but not adequately absorbed

• ex: meningitis, arachnoid villi dysfunction

overproduction (hydrocephalus)

• overproduction of CSF

• ex: choroid plexus tumors

characteristics of hydrocephalus:

• increased amount of CSF in brain’s ventricles

• enlargment of ventricles due to CSF accum

• increased ICP which causes headaches, vomiting, or changes in vision

stroke

• acute focal neurological deficit caused by vascular disorder resulting injury to brain tissue

• occurs when blood flow to region of brain is interrupted or when cerebral bv ruptures

• types: ischemic, hemorrhagic

ischemic stroke

• acute neurological deficit causing brain tissue injury

• cause: interruption or blockage of blood flow within cerebral artery

• results in reduced oxygen + nutrient delivery to brain tissue

ischemic stroke results from:

• thrombosis: the formation of a blood clot (called a thrombus) inside a blood vessel or heart chamber, which slows or blocks normal blood flow

• embolism: when a traveling substance—such as a blood clot, fat, air bubble, or amniotic fluid—gets stuck in a blood vessel and blocks normal blood flow

transient ischemic attack (TIA)

• temp interruption of cerebral blood flow

• similar causes to ischemic stroke: atherosclerosis

• symptoms (similar to stroke) resolve within minutes to hours

• no perm brain damage occurs

picture of TIA and ischemic stroke

thrombotic stroke (ischemic stroke)

• caused by blood clot formation within cerebral arteries

• slow onset of neurological symptoms

• associated w/ atherosclerosis

lacunar stroke (ischemic stroke)

• small vessel ischemic stroke affecting deep brain structures (basal ganglia, brain stem)

• often due to chronic hypertension causing small vessel disease

embolic stroke (ischemic stroke)

• caused by traveling blood clot (embolus)

• occurs when clot or debris travels through bloodstream to brain

• sudden onset of neurological symptoms

• emboli originate from: thrombus in left atrium or ventricle

hemorrhagic stroke

• cerebral blood vessel rupture causes bleeding in and around the brain tissue and spaces

• caused by rupture of cerebral bv, resulting in bleeding within or around brain

• causes brain injury due to: comrpession, swelling (edema), increased ICP

• two types: intracerebral, subarachnoid

intracerebral hemorrhage (hemorrhagic stroke)

bleeding directly into brain tissue

subarachnoid hemorrhage (hemorrhagic stroke)

bleeding into space arachnoid and pia mater, often due to ruptured aneurysm

picture of risk factors

picture of stroke manifestations !!

motor deficits with strokes:

• most common consequence of a stroke

• damage of corticospinal tract causes weakness on contralateral side of body

initial phase of stroke-related motor deficits

• flaccidity (decreased muscle tone)

• severe weakness

recovery phase of stroke-related motor deficits

• 6-8 weeks

• hyperreflexia develops

• spasticity replaces flaccidity

stroke-related dysathria

• stroke-related, communication disorders after stroke

• impaired articulation of speech sounds

  • changes in voice quality or pitch

  • results from weakness of muscles controlling pharynx, palate, tongue, lips

  • doesn’t affect language comprehension

stroke-related aphasia

• stroke-related, communication disorders after stroke

• decline in speech and language comprehension

seizure

• sudden, transient disruption in brain electrical function caused by abnormal excessive discharges of cortical neurons

• symptoms of disease, but no specific disease

• associated w/ metabolic derangements, infections brain tumors, drug abuse, vascular lesions

• single ep of abnormal neuronal discharge

• divided into focal and generalized

epilepsy

• recurrence of seizures and disorder for which no cause can be found

• chronic neurological disorder

• characterized by recurrent seizures

focal seizure

• begin in specific (focal) area of one cerebral hemisphere

• symptoms depend on location of affected brain region

• may remain localized or spread to other areas

• can classify into: focal aware, focal impaired awareness

focal aware seizures

• consciousness remains intact

• symptoms: depend on area, but can include: jerking of limb, tingling sensations, visual or auditory disturbances, emotional changes

focal impaired awareness seizures

• altered or impaired consciousness

• may involve automatisms like: lip smacking, chewing, repetitive hand movements, often followed by confusion

generalized seizures

• begin simultaneously in both cerebral hemispheres

• involve widespread brain activity from onset

• usually affect consciousness + may produce bilateral motor symptoms

• classifies into: absence, tonic, clonic, tonic-clonic, status epilepticus

absence generalized seizure

• brief loss of awareness

• common in children, usually last a few seconds

tonic generalized seizure

sudden muscle stiffening that may cause falls

clonic generalized seizure

repetitive rhythmic jerking movements

tonic-clonic generalized seizure

• most common type

• tonic phase: muscle stiffening

• clonic phase: rhythmic jerking

• often followed by postictal period of confusion + fatigue

status epilepticus generalized seizure

• continuing/recurring seizures w/ incomplete recovery, unrelenting seizure activity that lasts 30 mins or more

• medical emergency

seizure sequence

• prodromal phase: occurs before some seizures

• aura phase: earliest symptoms of seizure

  • common symptoms: unsual smells, taste, or sound

• ictal phase (seizure event): period of active seizure

• postictal phase: recovery phase following seizure

  • exhaustion, headache, weakness, confusion

dementia

• chronic, progressive decline in cognitive function

• decreased cortical function leads to range of cognitive and behavioral impairments, including:

  • impaired cognitive skills, impaired thinking, judgment, learning, memory loss, confusion, personality changes

• common types of dementia: alzheimer’s disease, vascular dementia, lewy body dementia (dementia associated with advanced PD)

alzheimer’s disease

• progressive cortical atrophy

• accumulation of beta-amyloid plaques between neurons

• formation of neurofibrillary tangles (tau proteins) inside neurons

• neuronal damage + brain atrophy, especially in hippocampus, and reduced lvls of acetylcholine (neurotransmitter for memory)

• cause unknown, but risk factors include advanced age, genetics/history

picture of alzheimer disease

early signs for alzheimer’s disease (AD)

• impaired learning, poor judgment

• mild memory loss of recent events

• difficulty finding words

middle and advances stages for alzheimer’s disease (AD)

• behavioral changes

• increased confusion and disorientation

• difficulty recognizing familiar people

• gradual loss of memory and lack of concentration

• decline of cognitive function, and language