Ch 16 - Disorders of Brain Function

Three main parts of the brain (cerebrum, cerebellum, and brainstem)

Cerebrum → divided into 2 cerebral hemispheres

Cerebellum → little brain, coordinating execution and maintaining balance

Brainstem → divided into the midbrain, pons, and medulla oblongata

Protective structures of the brain

• cranial meninges and associated spaces

• cranial bones

Cerebral circulation

delivers oxygen and nutrients for its metabolic needs and to remove carbon dioxide and other waste products

Diencephelaon

thalamas, hypothalamus, and epithalamus

Cranial Meninges (Dura Mater. arachnoid mater, and pia mater)

dura mater: outermost layer of the cranial meninges (thick, tough membrane)

arachnoid mater: middle layer that lies directly below the dura mater, is very delicate

subarachnoid space: contains CSF and lies between the arachnoid and pia

pia mater: inner most layer; very thin, delicate membrane that over the brain surface

Falx Cerebri

fold of dura between the right and left cerebrum

Cerebral Circulation

1. circle of willis - network of brain arteries that provides alternative pathways for blood flow in case of blockage

2. superior sagittal sinus

3. inferior sagittal sinus

structures of cerebral circulation

Cerebral Aqueduct

a narrow, fluid-filled channel located within the midbrain that connects the third ventricle to the fourth ventricle

Focal Brain injury

caused localized neurologic defects

• brain injuries are based on how much tissue is damaged

• the symptoms correspond to the injured brain region

Global brain injury

affect the entire brain

• usually results in altered consciousness

What are brain injuries manifested by?

• changes in the level of consciousness

• alternations in cognitive function

• motor dysfunction

• sensory impairment

Coup-countercoup injury

traumatic brain injury

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

coup injury → occurs directly beneath the site where the head is struck

• person is hit in the forehead

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

• this is PRIMARY IMPACT

countercoup injury → occurs at the side opposite of impact (brain moves back)

• after striking the front of the skull, the brain rebounds backward

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

• this is SECONDARY IMPACT

Concussion

traumatic brain injury

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

• no structural brain damage visible to imaging

• temporary neurological dysfunction

• may involve brief loss of consciousness or none at all

signs and symptoms

• headache, dizziness, and confusion

• amnesia → memory loss

• nausea and vomiting

• blurred vision and sensitivity to light or noise

the patient requires monitoring

after any trauma, the secondary injury or complications are more common

Contusion

traumatic brain injury

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

• more severe than a concussion

• involves hemorrhage, edema, tissue injury, and hypoxia

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

signs and symptoms

• signs of increased intracranial pressure

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

• seizures, weakness or paralysis

Reticular activating system (RAS)

network of neurons located in the brainstem (midbrain, pons, and medulla)

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

• receives sensory input from visual, auditory, and tactile sensory pathways

• transmits activating impulses from the brainstem to the thalamus, hypothalamus, and cerebral cortex

• signals increase cortical activity, enabling awareness, attention, and wakefulness

Level of Consciousness (LOC)

refers to a degree of awareness of self and the environmental and ability to respond to stimuli

Full consciousness

fully awake and aware

• responds appropriately to environmental stimuli

• oriented to person, place, time, and situation

Confusion

awake but disoriented

• difficulty thinking clearly or following commands

• responds may be slow or inappropriate

Lethargy

drowsy and sleepy

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

• responds appropriately to painful stimuli (person has normal withdrawal reflex)

Obtundation

decreased alertness and interest in the environment (deeper than lethargy → more sleepy but cannot respond to directions)

• requires repeated verbal stimulation to maintain attention

• responses are slower and less accurate

Stupor

can only be aroused by vigorous or painful stimuli

• minimal verbal responses

• returns to an unresponsive state when stimulation stops

Coma

completely unconscious

• sleeplike state with eyes closed

• cannot be awoke by any means

Glasgow Coma Scale (GCS)

neurological scoring system used to assess level of consciousness 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

• motor response is response to painful stimulus

total score

GCS = E + V + M

maximum → 15 (fully altert)

minimum → 3 (deep coma)

Decorticate deterioration

appearance

• flexion of the arms, wrists, and fingers

• arms are adducted toward the body

• lower extremities internally rotated

• feet plantar-flexed

cause

• lesions of the cerebral hemispheres

• damage to the internal capsule

in the cerebral cortex; damage of upper motor neurons in the cerebral cortex and thalamus

Decerebrate deteriorating brain function

appearance

• arms rigid and extended

• palms turned away from the body

• legs stiffly extended

• feet are plantar-flexed

cause

• lesions involve the diencephalon, midbrain, and upper brainstem

• associated with poorer prognosis

more severe, affects respiratory and cardiovascular centers

can also have damage to cerebral cortex; the injury is in the lowest portion but can be in the cerebral cortex

Brain Death

irreversible loss of function of the entire brain, including the brainstem

• the body cannot maintain internal homeostasis

there is no consciousness, no brainstem reflexes, no ability to breathe independently

Cerebral death

irreversible loss of function of the cerebral hemispheres, brainstem function is present

• damage of the neurons in the cerebrum

there is no awareness or higher mental function, the brainstem might still control breathing, heart rate, and reflexes

Brain injury

occurs when the brain tissue is damaged by a physical force, loss of blood flow, lack of oxygen, infection, and toxins

Primary injury

immediate damage occurs at the time of the insult

• loss of neurons and glial cells, bleeding, and impulses are not sent

ex) head trauma causing bruising or tearing of brain tissue

mechanisms of primary injury

• mechanical disruption of neurons and glial cells

• tearing of axons → diffuse axonal injury

• direct injury to blood vessels

secondary brain injury

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

mechanism of brain injurt

Ischemia and Hypoxia

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

• ATP production falls (b/c of less oxygen)

• ion pumps fail, causing cellular swelling and dysfunction

mechanism of brain injury, causes secondary brain injury

Excitotoxicity

injured neurons release excessive amounts of the neurotransmitter glutamate

• glutamate stimulates NMDA and AMPA receptors

• excess calcium enters the cells → leads to activation of enzymes

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

mechanism of brain injury, causes secondary brain injury

Glutamate

principal excitatory NT in the brain

• prolonged ischemia results in glucose transporters become immobilized and ineffective

the excess glutamate binds to receptors, opens channel for Ca2+, Ca2+ activates metabolism inside the cell

1. increase in intracellular calcium

2. calcium cascade

3. release of intracellular enzymes, protein breakdown, free radical formation, lipid peroxidation, fragmentation of DNA, nulear breakdown, brain cell injury and death

slide 28 → go back

CSF

clear colorless fluids that surrounds and protects the brain and SC

• provides buoyancy → to reduce weight of the brain

CSF is produced in the ventricles by the choroid plexus

CSF goes into the subarachnoid space through two openings in the fourth ventricle (the median aperture (foramen of magendie) and lateral aperture)

• CSF is reabsorbed by the arachnoid villi in the superior sagittal sinus and returned to the blood

Pathway of CSF

1. Lateral ventricle

2. Third ventricle

3. fourth ventricle

4. subarachnoid space

5. arachnoid villi

6. blood

Intracranial pressure (ICP)

pressure exerted by the contents of the cranial cavity

reflects the balance between

• the brain tissue (80%)

• cerebral blood volume (10%)

• cerebrospinal fluid (10%)

  • any change in ICP can be balanced by other 2 compartments, must be compensated by a decrease in one or both of the others; if they don’t, the ICP rises (bad)

the total intracranial volume remains constant, normal ICP for an adult is 5-15 mmHg

Monro-Kellie hypothesis

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

• change (e.g., increases) in one component is balanced by an equal and opposite effect (e.g., decrease) in one or both of the remaining components

Cerebral perfusion pressure (CPP)

the blood only reaches the brain when the CCP is adequate

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

MAP = pressure pushing blood into the brain

ICP = pressure opposing blood entry into the brain

What happens when ICP rises?

compression of cerebral BVs occurs

CPP decreases (leading to no blood reaching the brain)

cerebral blood flow falls

brain tissue receives less oxygen and glucose

cerebral ischemia and neuronal injury develop

displacement of some parts of the brain

• hypoxia and decreased metabolism

Brain herniation

the displacement of brain tissue form its normal position due to increase intracranial pressure, causing it to move across rigid intracranial structure suchs as the falx cerebri, tentorium cerebelli, or foramen magnum

• life threatening neurological emernecy

• compression of vital brain structures and BVs

common causes

• traumatic brain injury

• intracranial hemorrhage

• brain tumors

Cingulate brain herniation

cingulate gyrus is pushed beneath the falx cerebri

• may compress the anterior cerebral artery (brings O2 to motor areas)

• signs: unilateral or bilateral leg weakness

Uncal brain herniation

medial temporal lobe (uncus) herniates through the tentorial notch

• compresses the ipsilateral third cranial nerve (oculomotor)

• signs: dilated, fixed ipsilateral pupil, decreased consciousness

Central brain herniation

downward displacement of the diencephalon, brainstem, and forneum magnum

• signs: progressive loss of consciousness, decorticate posturing

Hydrocephalus (noncommunicating, communicating, and overproduction)

condition in which excessive CSF accumulates within the ventricles of the brain

three types:

noncommunicating → CSF flow is blocked within the ventricular system

• typically at birth (congential)

• ex) aqueductal stenosis, tumors, congential malformations

communicating → CSF reaches the subarachnoid space but is not adequately absorbed

• has impared absorption into superior sagittal sinus

• ex) meningitis, arachnoid villi dysfunction

overproduction → excess CSF dysfunction

• ex) choroid plexus tumors

Pathogenesis of hydrocephalus

1. increased amount of CSF in the brain’s ventricles

2. enlargements of the ventricles due to CSF accumulation

3. increased ICP which can cause headaches,, vomiting, or changes in vision

Hematoma

results from injury to blood vessels and subsequent bleeding

blood can accumulate within different compartments of the skull

Epidural hemotatoma

collection of blood between the inner surface of the skull and the dura mater

• caused by rupture of the middle meningeal artery

• manifestations: severe headache, nausea, vomiting, loss of consciousness

• has a very fast development (within hours)

Subdural Hemotaoms

collection of blood between the dura mater and the arachnoid mater

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

• slow bleeding (days-weeks)

• more common in older people

• manifestations similar to epidural hematoma

mechanisms of bleeding: severance of bridging veins, subfalcine herniation, threat of transtenorial herniation

Intracerebral Hematoma

collection of blood within the brain tissue

• results from severe movements of the brain during head trauma or progression of a cerebral contusion into a hematoma

• manifestations vary depending on the size and location of the hematoma

Stroke

acute focal neurological deficit caused by a vascular disorder that results in injury to the brain tissue

• occurs when blood flow to a region of the brain is interrupted or when a cerebral vessel ruptures

Ischemic stroke

87% of all strokes

• caused by an interruption or blockage of blood flow within a cerebral artery

• results in reduced oxygen and nutrient delivery to brain tissue

• is considered a “true stroke"“

• >60 minutes

results from:

thrombosis → clot formation in the vessel

embolism → clot traveling from elsewhere (moves and blocks a cerebral artery)

Hemorrhagic stoke

13% of all stroke, more severe (usually fatal)

• caused by a rupture of a cerebral blood vessel, resulting in bleeding within or around the brain

Transient Ischemic Attack (TIA)

temporary interruption of cerebral blood flow

• caused by atheroscelrois, emboli

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

• no permanent brain damage occurs

• narrowing or blockage is removed

<60 minutes

Thrombotic Stroke

ischemic stoke caused by blood clot formation within cerebral arteries

• most common cause of ischemic stroke

• slow onset of neurological symptoms

• associated with atherosclerosis (bc atherloscleortic plaque ruptures or progresses, thrombus at the site of narrowing, blood flow becomes blocked)

• localized → may be less permanent damage if collateral circulation as been established

Lacunar Stroke

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

• localized area of stroke

• often due to chronic hypertension causing small vessel disease

Embolic Stroke

ischemic stroke caused by a traveling blood clot (embolus)

• occurs when a clot or debris travels through the bloodsteam to the brain

• blocks a cerebral artery, leading to sudden brain ischemia and neurological deficits

• sudden onset

• has minimal increase ICP effects, is localized until multiple emboli are present

most emboli originate from:

• thrombus in the left atrium or left ventricle

• atherosclerotic plaques in the carotid arteries

atrial fibrillation

twitching of atria that can lead to formation of blood clots

What is the #1 risk factor of an ischemic stroke?

athlerosclerosis in cerebral and carotid arteries

Hemorrhagic Stroke (+ intracerebral and subarachnoid)

occurs when a cerebral blood vessel ruptures

• frequently fatal type of stoke

• blood leaks into the brain tissue or surrounding spaces

• causes brain injury due to: compression, swelling, increased ICP

• usually develops because of HTN

two main types:

1. intracerebral hemorrhage → bleeding directly into the brain tissue

2. subarachnoid hemorrhage → bleeding ito the space between the arachnoid and pia mater, often leading to a rupture aneurysm (100% fatal)

Ischemic stoke risk factors

• HTN

• atrial fibrillation

• diabetes

• high cholesterol

• smoking

• carotid artery atherosclerosis (narrowing)

Hemorrhagic Stroke risk factors

• uncontrolled HTN

• brain aneurysms

• arteriovenous malformations (AVMs)

• use of anticoagulants (blood thinners)

• heavy alcohol consumption

Ischemic Stroke Manifestations

often related to loss of blood flow to a specific brain area

• sudden unilateral weakness or paralysis

• facial droop

• numbness on one side

• difficulty speaking or understanding speech

• vision loss or double vision

• difficulty walking or maintaining balance

• usually no severe headache

Hemorrhagic Stroke manifestations

often related to bleeding and increased pressure inside the skull

• sudden neurological deficits (weakness, speech problems)

• sudden severe headache

• nausea and vomiting

• decreased lvl of consciousness

• neck stiffness (especially with subarachnoid hemorrhage)

• rapid neurological deterioration

Left and right brain damage

left brain damage → right side paralysis, speech and memory deficits, cautions and slow behavior

right brain damage → left side paralysis, perceptual and memory deficits, quick and impulsive behavior

initial phase and recovery phase of stroke related motor deficits

initial phase

• flaccidity (decreased muscle done)

• severe weakness

recovery phase (6-8 weeks)

• hyperreflexia develops

• spasticity replaces flaccidity

Dysarthria and Aphasia

communication disorders after stroke

dysarthria - impaired articulation of speech sounds

• changes in voice quality or pitch

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

• does not affect language comprehension or content

aphasia → impaired ability to comprehend, integrate, and express language

Seizure

sudden, transiet disruption in brain electrical function caused by abnormal excessive discharged of cortical neurons (brain neurons fire more signals than they should)

• symptom of disease, not a specific disease

  • associated with metabolic derangements, infections brain tumors, drug abuse, and vascular lesions

• a single episode of abnormal neuronal discharge

Epilespy

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

• chronic neurological disorder

• characterized by recurrent seizures

• result of abnormal electrical activity in the brain

Focal and Generalized seizures

seizure classifications

focal → begin in a specific (focal) area of one cerebral hemisphere

• symptoms depend ono the loco of affected brain region

• may remain local or spread to other areas

generalized → begins simultaneously in BOTH cerebral hemispheres

• involves widespread brain activity from the onset

• usually affect consciousness and may produce bilateral motor symptoms

Focal aware seizures and focal impaired awareness seizures

Focal Aware Seizures: consciousness remains intact

• symptoms depend on the affected brain area: jerking of a limb, tingling sensations, visual or auditory disturbances, emotional changes

Focal impaired awareness seizures: altered or impaired consciousness

• involves automatisms such as lip smacking, chewing, repetitive hand movmenets

• often followed by confusion

Absence

brief loss of awareness

• common in children, usually lasting a few seconds

seizure classification

Tonic

sudden muscle stiffening that may cause fallsc

clonic

repetitive rhythmic jerking movements

Tonic-clonic seizures

most common type

• tonic phase: muscle stiffening

• clonic phase: rhythmic jerking

• often followed by a postictal period of confusion and fatigue

Status Epilepticus

continuing/recurring seizures within incomplete recovery, unrelenting seizure activity that lasts 30 minutes or more

• medical emergency

Seizure sequence (prodromal phase, aura, ictal, and postictal)

1. prodromal phase - occurs before any seizures

2. aura phase - earliest symptom of a seizure (common symptoms: unusual smells, tastes, or sounds)

3. ictal phase (seizure event): period of active seizure activity

4. postictal phase: recovery period following the seizure (common symptoms: confusion, fatigue, and headache)

Dementia

chronic, progressive decline in cognitive function

• leads to:

  • impaired cognitive skills

  • impaired thinking, judgement, and learning

  • memory loss, confusion

  • behavioral and personality changes

common types:

1. Alzheimer’s Disease → most common

2. Vascular Dementia → due to reduced blood flow to the brain

3. Lewy body dementia → dementia that develops in advanced stages of parkinsons

Alzheimers Disease

progressive cortical atrophy

• accumulation of beta-amyloid plaques between neurons

• formation of neurofibrillary tangles (tau proteins) inside neurons

• neuronal damage and brain atrophy, especially in the hippocampus

• reduced level of ACh (important for memory)

specific cause is unknown, risk factors:

• advanced age (most important)

• family history/genetics

Signs and symptoms of Alzheimers Disease

they extend over 10 to 20 years

early signs

• impaired learning, poor judgement

• mild memory loss of recent events

• difficulty finding words

middle and advanced stages

• behavioral changes → irritability, hostility, and mood swings

• increased confusion + disorientation'

• difficulty recognizing familiar people

• gradual loss of memory and lack of concentration

• decline of cognitive function, and language

• lack of environmental awareness, incontinence, and inability to function

Testing and treatment for alzheimers disease

no definitie diagnostic testing available

• exclusion of other disorders

• careful medical and psychological history

treatment

• no specific treatment

• anti cholinesterase drugs show some temporary improvements

• occupational therapists, psychologists, speech therpay

• teams approach needed to support client and caregivers