Neurologic Function

cerebral cortex

receives sensory information from skin, muscles, glands, and organs; sends message to move skeletal muscles; thinking, learning, remembering, and integrates nerve impulses

basal nuclei

coordination of slow, sustained movements and suppress useless patterns of movement

thalamus

relays most sensory information from the spinal cord and certain parts of the brain to the cerebral cortex; interprets certain sensory messages such as those of pain, temperature, and pressure

hypothalamus

controls various homeostatic functions such as body temperature, respiration, and heart rate; directs hormone secretions of the pituitary

cerebellum

coordinates subconscious movements of skeletal muscles; contributes to muscle tone, posture, balance, and equillibrium

brainstem

cranial nerves; reflex center for eyeballs, head, and trunk; regulates heart rate and breathing; plays a role in consciousness; transmits impulses between brain and spinal cord

hydrocephalus

CSF accumulation within the skull, ventricles dilate and blood vessels become compressed, pressure thins the cortex causing severe brain damage; present at birth or develop later in life

causes of hydrocephalus

CSF flow disruption (obstructive hydrocephalus), or CSF is not properly absorbed by the bloodstream

risk factors of hydrocephalus

prematurity, pregnancy complications, other congenital defects, NS tumors, CNS infections, and severe head injuries

hydrocephalus in infants

large head, rapid increase in head size, bulging fontanelle, seizures, development delay

hydrocephalus in older children and adults

headache followed by vomiting and nausea, blurred vision or diplopia, sluggish pupil response to light, uncoordinated movements, extreme fatigue, development delay, memory loss, confusion, irritability, personality changes

spina bifida

posterior spinous process on the vertebrae fail to fuse, permitting the meninges and spinal cord to herniate, most common birth defect in the US

maternal risk factors of spina bifida

family history of neural defects, folate deficiency, certain med, diabetes mellitus

complications of spina bifida

physical and neurologic impairments, hydrocephalus, meningitis, and learning problems

spina bifida occulta

mildest form, small gap in or more vertebrae, defect may not be evident other than a dimple or birthmark or tuft of hair over the site

meningocele (spina bifida)

rare form that involves the same bony defect as in spina bifida occulta but the meninges protrude through the vertebral meaning; meninges and CSF form a sac on the surface of the back, spinal cord develops normally and no neurologic impairment is usually not present

myelomeningocele

spinal canal remains open along several vertebrae in the lower or middle back; the meninges, spinal cord, spinal nerves, and CSF protrude through the large opening and form a sac on the infant’s back; tissues and nerves exposed in most cases, most sever form

complications of myelomeningocele

neurologic impairment, bowel and bladder problems, seizures, and other medical complications

cerebral palsy

nonprogressive disorders that appear in infancy or early childhood and permanently affect motor movement and muscle coordination

cerebral palsy causes

damage to the cerebellum during the prenatal period or during childbirth, but can occur at any time during the first 3 years of life, when the brain is developing

contributing factors of cerebral palsy

prematurity, low birth weight, breech births, multiple fetuses, hypoxia, cerebral hemorrhage, neurologic infections, head injury, maternal infection during pregnancy, maternal exposure toxins during pregnancy

manifestations of cerebral palsy

persistence of early reflexes, development delays, ataxia, spasticity, flaccidity, hyperreflexia, unusual positioning of limbs when resting or when held up, excessive drooling, difficulty swallowing, impaired sucking, and difficulty with fine motor skills

complications of cerebral palsy

balance and coordination issues, contractures, atrophy below the waist, speech delays, learning or cognition difficulties, seizures, urinary incontinence, constipation, chronic pain, and injury

meningitis

inflammation of meninges and subarachnoid space usually resulting from and infection leading to swelling of the meninges and increased intracranial pressure, self-limiting (viral) or life-threatening (acute bacterial)

causes of meningitis

bacteria, viruses, tumors, allergens

manifestations of meningitis

fever, chills, mental status changes, decreased consciousness, nausea, vomiting, photophobia, severe headache, stiff neck, agitations, bulging fontanelle

complications of meningitis

permanent neurologic damage, paralysis, seizures, hearing loss, blindness, speech difficulties, learning disabilities, behavior problems, acute renal failure, cerebral edema, shock, and death

encephalitis

inflammation of the brain and spinal cord usually resulting from infection; infection triggers inflammatory response that causes vasodilation, increased capillary permeability, and leukocyte infiltration; can cause nerve cell degeneration and diffuse brain destruction

causes of encephalitis

viruses and bacterial infections

complications of encephalits

cerebral edema, cerebral hemorrhage, and brain damage

manifestations of encephalitis

similar to meningitis but with more gradual onset, history of flu like symptoms

zika virus

caused by flavivirus caused by transmission of mosquito, foreign travel, local mosquito spread, and sexual transmission

manifestations of zika virus

none usually but when present include flulike symptoms

complications of zika virus

rare but severe, with maternal-fetal transmission: ocular lesions, miscarriage, and microcephaly

traumatic brain injuries (TBI)

usually caused by a sudden and violent blow or jolt to the head or a penetrating head wound that disrupts the normal brain function; can bruise the brain, damage nerve fibers, and cause hemorrhaging

manifestations of traumatic brain injuries (TBI)

may be vague and insidious or sudden and severe, symptoms may improve and suddenly worsen, outward appearance of head is not an indication of injury severity, not being able to recall event details, indications of a concussion, changes in or unequal pupil size, seizures, asymmetrical facial features, fracture of skull or face, bruising of face, inability to move one or more limbs, irritability, personality changes, unusual behavior, loss of consciousness; fluid draining from nose, mouth, or ears

concussion

closed TBI, momentary interruption of brain function, results from a mild blow to the head that causes sudden movement of the brain and disrupting neurologic function; may or may not lead to loss of consciousness; amnesia, confusion, sleep disturbances, and headaches may occur for weeks

cerebral confusion

closed TBI, bruising of the brain, results from a blunt blow that causes the brain to make sudden impact with the skull, varies in severity depending on the extent of damage and the amount of bleeding residual effects depend on severity

coup

initial area where the brain impacts the skull during cerebral contusion

contrecoup

opposite side of the brain where it rebounds and impacts the skull

open TBIs

increased risk for infections — fractures: linear skull fracture, comminuted skull fracture, compound skull fracture, depressed skull fracture, basilar skull fracture

glasgow coma scale

assess and document level of consciousness in patients with head trauma; includes eye opening, verbal response, motor response, response to stimuli, posture

increase intracranial pressure

increased volume in limited space, blood vessels dilate to increase blood flow and constrict if ICP increases, delicate pressure-volume relationship between skull contents

monro-kellie hypothesis

an increase in one volume by a decrease in the volume of another, accomplished mostly by shifts in the CSF and blood volume (vasodilation/constriction)

normal intracranial pressure (ICP)

60-200

cushing’s reflex

increase sympathetic stimulation when the mean arterial pressure drops below the ICP; causes vasoconstriction, increased cardiac contractility, and increased cardiac output

cushings triad

increased blood pressure, bradycardia, and cheyne-stokes respirations

herniations

complication of increased ICP, compress neural tissue and cranial nerves, can lead to mild or severe issues — compression of reticular activation system in brainstem can lead to coma or death; can affect different parts of brain, brainstem, or cerebellum; manifestations depend on which region of the brain/nerves is compressed

intracranial hemotomas

collection of blood in the tissue that develops from ruptured blood vessels, can develop immediately or slowly because of a TBI, bleeding leads to localized pressure on nearby tissue and increases ICP, blood may coagulate and form a solid mass

epidural hematoma

result from bleeding between the dura and skull, usually caused by and arterial tear; brief loss of consciousness, followed by a short period of alertness, then loss of consciousness again

manifestations of epidural hematomas

include marked neurologic dysfunction that usually develops within a few hours of injury

subdural hematoma

develop between dura and arachnoid, frequently caused by a small venous tear, generally developed slowly (within 24 hours), progress rapidly and have high mortality, ICP increases over a period of about a week after the injury

manifestations of subdural hematoma

develop several weeks after the injury because of a slow leak, more common in elderly adults because of brain atrophy

intracerebral hematomas

result from bleeding in the brain tissue itself; caused by contusion or shearing injuries but can also result from hypertension, cerebral vascular accidents (strokes), aneurysms, or vascular abnormalities

subarachnoid hemorrhage

results from bleeding in the space between the arachnoid and pia; primary clinical presentation is a severe headache with a sudden onset and that is worse near the back of the head

spinal cord injuries

result from direct injury to the spinal cord or indirectly from damage to surrounding bones, tissues, or blood vessels

direct damage in spinal cord injuries

can occur if the spinal cord is pulled, pressed sideways, or compressed

indirect dammage in spinal cord injuries

results from the accumulation of blood or fluid can compress the spinal cord and damage it

causes of spinal cord injuries

motor vehicle accidents, falls, violence, sports injuries, and weakening vertebral structures

spinal shock

spinal cord injury; temporary suppression of neurologic function because of spinal cord compression, neurologic function gradually returns

autonomic hyperreflexia

spinal cord injury; massive sympathetic response that can cause headaches, hypertension, tachycardia, seizures, stroke, and death; most commonly associated ith injuries above T6

neurogenic shock

spinal cord injury; an abnormal vasomotor response secondary to disruption of sympathetic impulses

manifestations of spinal cord injuries

loss of neurologic functioning, varying degrees of paralysis

manifestations in cervical/thoracic spinal cord injuries

affect upper and lower extremities; breathing difficulties, loss of normal bowel and bladder control, paresthesia, sensory changes, spasticity, pain, weakness, paralysis, blood pressure instability, temperature fluctuations, and diaphoresis

manifestations in lumbar/sacral spinal cord injuries

affect the lower extremities in varying degrees, similar to cervical injuries with the exception of cervical injuries

complications of spinal cord injuries

respiratory failure, effects of immobility (constipation, pulmonary infections, urinary infections, thrombus, impaired skin integrity, contractures), changes in bowel and bladder function, sexual dysfunction, chronic pain, death

transient ischemia attack (TIA)

mini stroke, temporary episode of cerebral ischemia that results in symptoms of neurologic deficits, lasts 1-2 hours → up to 24 hours, begin suddenly and last for a short period, 1 in 3 people eventually have a stroke

causes of transient ischemia attack

cerebral artery occlusion, cerebral artery narrowing, and cerebral artery injury

risk factors of transient ischemia attack (TIA)

smoking, diabetes mellitus, advancing age, hypercholesterolemia, excessive alcohol consumption, and ilicit drug use

cerebral vascular accident (CVA)

stroke, interruption of cerebral blood supply, ischemic drug is permanent

ischemic stroke (type of CVA)

most common, total vessel occlusion (thrombus, embolus, or plaque)

hemorrhagic strokes

most fatal, cerebral vessel rupture (cerebral aneurysm, arteriovenous malformation, or hypertension)

complications of cerebral vascular accident (CVA)

neurologic deficits and death

risk factors of cerebral vascular accident (CVA)

smoking, diabetes mellitus, advancing age, hypercholesterolemia, excessive alcohol consumption, and illicit drug use