BIO 210 Chapter 14 (Neuro.)

expanding lesions in brain

caused by growing tumor or hemorrhage. additional impairment is noted as adjacent areas become involved

paresis

weakness

Supratentorial lesions

occur in the cerebral hemispheres above the tentorium cerebelli. leads to specific dysfunction in a discrete area

Infratentorial lesions

located in brainstem/ below the tentorium. may affect many motor and sensory fibers (resulting in widespread impairment). respiratory/ circulatory function & level of consciousness may be impaired

damage to left hemisphere

Loss of logical thinking ability, analytical skills, other intellectual abilities, communication skills

damage to right hemisphere

impairs appreciation of music and art, Causes behavioral problems, Spatial orientation and recognition of relationships may be deficient & self care deficits are common

deterioration of levels of consciousness

decreased level of responsiveness, reduced consciousness, vegetative state, locked in syndrome, brain death

levels of reduced consciousness may lead to...

confusion, disorientation, memory loss, unresponsive to verbal stimuli, difficulty in arousal, loss of consciousness/ coma

vegitative state

loss of awareness & mental capabilities. result of diffuse brain damage. brainstem function continues. appearance of sleep - wake cycle. person is unresponsive to external stimuli

brainstem

keeps us alive

Locked-in syndrome

Individual is aware and capable of thinking but is paralyzed and cannot communicate

criteria for brain death

Cessation of brain function (Including function of the cortex and the brainstem, Flat or inactive EEG), Absence of brainstem responses, Absence of spontaneous respirations when ventilator assistance is withdrawn, Evaluated twice by different physicians

damage to upper motor neurons

Interference with voluntary movements, Weakness or paralysis on the contralateral side of the body

spastic paralysis (upper motor neuron damage)

limb has hyperflexia

damage to lower motor neurons

Weakness or paralysis on the same side of the body. At and below the level of spinal cord damage

flaccid paralysis (lower motor neuron damage)

mushy muscle tone & no tendon reflex

decorticate & decerebrate posturing

indicates severe brain damage

sensory deficits

involves touch, pain, temperature, position, special senses of vision/ hearing/ taste/ smell

somatosensory cortex

area at the front of the parietal lobes that receives and localized sensory input

hemianopia

visual loss

optic chiasm damage

vision is lost in both eyes if chiasm is totally destroyed. partial loss depends on particular fibers damaged

optic tract or occipital lobe damage

Loss of the visual field on side opposite to that of the damage

aphasia

inability to comprehend or express language

Dysarthira

motor function affecting muscles used in speech. words cannot be articulated clearly. usually results from cranial nerve damage or muscle impairment

agraphia

impaired writing ability

alexia

impaired reading ability

agnosia

loss of recognition or association

Seizures (convulsions)

Caused by spontaneous excessive discharge of neurons. results in abnormal sensory/ motor activity and possible loss of consciousness. manifested by involuntary repetitive movements or abnormal sensations/ hallucinations

Causes of seizures

trauma, infection, inflammation, hypoxia, bleeding in brain, fever, hypoglycemia (many idiopathic & could be congenital)

Triggers for seizures

physical stimuli (loud noise & bright light), biochemical stimuli (stress, hypoglycemia, excessive prementrual fluid retention, change in medication, hyperventilation)

absence seizure (generalized)

usually in children, lasting 5 - 10 seconds. brief loss of awareness and possible facial movements

tonic-clonic (grand mal) seizure (generalized)

aura, loss of consciousness, strong tonic muscle contractions (flexion & extension of limbs & trunk), jaw clenches

Clonic phase of tonic-clonic seizure

muscles alternately contract and relax

postictal phase of seizure

confusion, fatigue, sleep

simple partial seizure

arises from a single area of damage in the cerebral cortex & manifested as repeated motor activity

complex partial seizure

arise in the temporal lobe and possibly frontal lobe & limbic system. aura possible & seizure exhibits as bazaar behavior such as clapping or waving hands. possible visual/ auditorial hallucinations

continuous seizures

Increased metabolism of glucose and oxygen & May be life-threatening

Treatment of seziures

phenytoin (anti-convulsive drug) & phenobarbital (sedative)

increased intracranial pressure

a raised level of pressure within the skull

Increased ICP causes

ischemia & eventual infarction of the brain

Early signs of increased ICP

lethargy, decreased pupillary response, severe headache, vomiting, papilledema

as ICP increases, vasomotor centers:

respond in attempt to increase arterial blood supply to brain (crushing reflex) to combat cerebral ischemia

as ICP increases, systemic vasoconstriction:

increases systemic blood pressure & delivers more blood to brain to relieve ischemia

as ICP increases, baroreceptor response:

respond to increasing blood pressure by lowering heart rate

as ICP increases, chemoreceptor response:

respond to low carbon dioxide levels by reducing respiratory rate

visual signs of increased ICP

pressure on occulomotor nerve affects size & response of pupils. as pressure increases, pupils become fixed & dilated. droopy eyelid may occur

ptosis

drooping eyelid

herniation

brain is being pushed down

Transtentorial herniation

Cerebral hemispheres, diencephalon, midbrain are displaced downward. Resulting pressure affects flow of blood and CSF, RAS, and respiration

Uncal herniation

Uncus of the temporal lobe is displaced downward. Creates pressure on CN III, posterior cerebral artery, and RAS

intratentorial herniation

cerebellar tonsils are pushed down through the foramen magnum. compresses brainstem & vital centers. causes infarction and death

brain tumors

space-occupying lesions that cause increased ICP. both benign & metastatic can be life threatening

gliomas

primary malignant tumor of neuroglia cells. classified according to the cell derivation and location of tumor

primary brain tumor

starts at brain

secondary brain tumor

spreads to brain from breast or lung

occurrence of brain tumor in children

brainstem & cerebellar tumors are common

occurrence of brain tumors in adults

in cerebral hemispheres

clinical manifestations of brain tumor

increased ICP, vomiting, lethargy, headaches, personality/ behavior changes, seizures

brain tumor treatment

surgery, radiation, chemotherapy

vascular disorders of brain

could be hemorrhagic or ischemic

hemorrhagic vascular disorder

blood vessel bleeding/ ruptured

ischemic vascular disorder

blocked blood vessel

transient ischemic attacks (TIA)

mini stroke. temporary localized reduction of blood flow into brain tissue. recovers on it's own within 24 hours

pathophysiology of TIA

partial occlusion of an artery caused by atherosclerosis. small embolus. vascular spasm. loss of auto-regulation

clinical manifestations of TIA

intermittent short episodes of impaired function (muscle weakness in arm/ leg, visual disturbances, numbness in face, aphasia, confusion)

cerebrovascular accident (CVA)

stroke: infarction of brain tissue that results from lack of blood

pathophysiology of CVA

occlusion & rupture of cerebral blood vessel. 5 minutes of ischemia causes irreversible nerve cell damage. central area of necrosis surrounded by area of inflammation

risk factors for CVA (etiology)

Diabetes, Hypertension, Systemic Lupus Erythematosus, Atherosclerosis, History of TIAs, Increasing age, Obstructive sleep apnea, Heart disease, Smoking, Sedentary lifestyle, Combination of oral contraceptives and cigarette smoking, Congenital malformation of blood vessels

warning signs of CVA

weakness/ numbness in face/ arm/ leg/ one side of body, temporary loss of speech/ comprehension/ vision, sudden headache, unusual dizziness

treatment for CVA

clot busting agents, glucocorticoids to reduce brain swelling, surgical intervention to relieve artery obstruction, physical therapy/ rehabilitation

cerebral aneurysm

localized dilation of a cerebral artery (becomes weak & bursts)

pathophysiology of cerebral aneurysm

usually at points of bifurcation on circle of willis. often aggravated by hypertension. initially small and asymptomatic. slow bleeds cause headaches. ruptures leads to fatal increase of ICP and death

clinical manifestations of cerebral aneurysm

visual disturbances, photophobia, headache, nuchal rigidity, seizures, vomiting, loss of consciousness, death

treatment for cerebral aneurysm

surgical treatment before rupture & antihypertensive drugs

brain infections

meningitis, brain abscess, encephalitis, rabies

meningitis

bacterial infection within the meninges of CNS

pathophysiology of meningitis

Microorganism reach the brain via blood/ nearby tissue. Infections spread rapidly through CSF in subarachnoid space & the meninges. Inflammatory response leads to increased ICP. Exudate present in the CSF & can fill the sulci

clinical manifestations of meningitis

manifests quickly. severe headache, back pain, photophobia, nuchal rigidity (stiff neck), kernig sign (resistance to stretch leg), lethargy, elevated WBC (leukocytosis)

diagnostic tests for meningitis

Examination of CSF (obtained by lumbar puncture) & Identification of causative organism

treatment for meningitis

aggressive antimicrobial therapy & glucocorticoids for inflammation

brain abscess

localized infection in frontal or temporal lobes. usually necrosis of brain tissue & surrounding edema. may spread from organisms in ear, throat, lung & sinuses. surgical drainage & antimicrobial therapy needed

encephalitis

viral infection of the parenchymal/ connective tissue in brain & spinal cord. necrosis & inflammation develop in brain tissue, results in some permanent damage.

rabies

viral infection transmitted by bite of rabid animal or transplantation of contaminated tissue. virus travels along peripheral nerves to CNS; causes inflammation & necrosis in the brainstem

Tetanus (lockjaw)

caused by spores that enters through wound & enters nervous system. causes tonic muscle contractions, jaw stiffness, difficulty swallowing, stiff neck, headache, respiratory failure

Poliomyelitis (infantile paralysis)

virus that attacks motor neurons of spinal cord and medulla. causes fever, headache, vomiting, stiff neck, flaccid paralysis

postpolio syndrome

recurs 10-40 years after recovery from primary infection. patient experiences severe fatigue, weakness, pain & muscle atrophy

herpes zoster (shingles)

Caused by varicella-zoster virus in adults. Can occur years after primary infection of varicella (chickenpox). Usually affects cranial nerve or one dermatome (dormant). causes Pain, paresthesia (altered sensations), vesicular rash (lesion with clear fluid). If antiviral drugs started within 48 hours of onset, pain is significantly reduced. Lesions and pain persist for several weeks. Postherpetic pain may persist for months to years in some cases. (Vaccine available for those 60 years or older)

reyes syndrome

cause unknown but linked to viral infection. causes brain function to become impaired by cerebral edema. causes live to become enlarged & can result in acute failure

gullian-barre syndrome

ascending paralysis & progressive muscle weakness. inflammatory condition of PNS

concussion

minimal brain trauma

contusion

bruising of brain tissue causing rupture of small blood vessels & edema

closed head injury

brain tissue is injured but skill is not fractured

open head injury

Involve fractures or penetration of the brain

depressed skull fracture

Involve displacement of a piece of bone below the level of the skull, Compression of brain tissue (Blood supply to area often impaired—pressure to brain)

basilar fractures

occurs at base of skull with possible leakage of CSF through ears or nose

contrecoup injury

Area of the brain contralateral to the site of direct damage is injured, As brain bounces off the skull (May be secondary to acceleration or deceleration injuries)

direct brain injuries

Brain is lacerated, rupture of cerebral blood vessels. damage is caused in inner surface of the skull. movement of lobes against eachother

secondary brain injuries

Result from additional effects of cerebral edema, hemorrhage, hematoma, cerebral vasospasm, infection, ischemia related to systemic factors

trauma to brain tissue

Causes loss of function in part of body controlled by that area of the brain. Cell damage and bleeding lead to inflammation and vasospasm around injury site (Increased ICP, general ischemia, dysfunction)

types of hematomas in brain

epidural, subdural, subarachnoid, intracerebral