CH:16 patho

Consciousness is the

state of awareness of oneself and the environment

Awareness: encompasses all cognitive functions

arousal is the

state of awakeness

Supratentorial

produces changes by either diffuse or localized dysfunction. Above tentorium cerebelli

Infratentorial is

below tentorium cerebelli, destruction of reticular activating system, destruction of brainstem

Alert

patient responds immediately to minimal external stimuli

confused

patient is disoriented to time or place but usually oriented to person, with impaired judgment and decision-making and decreased attention span.

Delirious

Patient is disoriented to time, place, and person, with loss of contact with reality, and often has auditory or visual hallucinations.

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Lethargic

Patient needs an increased stimulus to be awakened.

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Obtunded

Patient displays dull indifference to external stimuli, and verbal response is minimal.

Stuporous

Patient can be aroused only by vigorous and continuous external stimuli. Motor response is often withdrawal or localizing to stimulus.

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Comatose

Vigorous stimulation fails to produce any voluntary neural response.

Metabolic is

alterations in delivery of energy, seen with hypoxia, electrolyte disturbances, hypoglycemia

Psychogenic (unresponsive)

uncommon, signal psychiatric disorders, despite apparent unconsciousness, person is physiologically awake.

Neurologic functions critical to evaluation of consciousness is

level of consciousness (most critical)

pattern of breathing

pupillary reaction

oculomotor responses

motor responses

A patient has a structural problem within the brain tissue that decreases the level of consciousness. Which of the following terms best describes this location?

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Intracerebral

Abnormal motor responses would include abnormal flexion which is

Decorticate posturing in midbrain injury

Abnormal extension- decerebrate posturing in brainstem injury

flaccid

Brain death means that the brain can no longer do what?

maintain internal homeostasis, irreversible

Brain death criteria would be

completion of all appropriate diagnostic and therapeutic procedures, unresponsive coma, no spontaneous respirations, no brainstem functions, flat EEG, persistence of signs for appropriate period

Cerebral death is an

irreversible coma, death of the cerebral hemispheres exclusive of the brain stem and cerebellum. No behavioral or environmental responses, brainstem can continue to maintain internal homeostasis

Survivors of cerebral death remain in what?

coma, they emerge into a persistent vegetative state, progress into a minimally conscious state, lock-in syndrome

Selective attention

ability to select from available, competing environmental and internal stimuli

Selective attention deficit is

temporary, permanent, or progressive

pathophysiologic mechanism is

direct destruction caused by ischemia and hypoxia or indirect destruction caused by compression.

effects of toxins, chemicals, or metabolic disorders

sensory inattentiveness

extinction, neglect syndrome

agnosia is a defect of

pattern recognition. Tactile, visual, or auditory. Failure to recognize form and nature of objects.

aphasia is

defect of language comprehension or production, usually associated with cerebrovascular accident

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Acute confusional states is

transient disorders of cognitive function, consciousness, or perception. arise from brain networks, not a discrete area of the brain.

Delirium is

hyperactive and hypoactive

Dementia is a progressive failure of

many cerebral functions including impairment of intellectual processes. Losses of orientation, memory, language, judgement, and decision making

mechanisms for dementia include

neuron degeneration, brain tissue compression, atherosclerosis, brain trauma, infection and neuroinflammation.

Alzheimer’s disease is

the leading cause of severe cognitive dysfunction in older persons

* cause is unknown
* nonhereditary sporadic or late onset AD, early-onset familial AD, early onset AD

Pathologic alterations for alzheimers is

neuritic plaques, neurofibrillary tangles

Clinical manifestations for alzheimer’s disease is

early: forgetfulness, emotional upset

Over time: memory loss, disorientation, confusion, lack of concentration, decline in abstraction, problem solving, and judgment

Diagnosis of alzheimer’s is made by

ruling out other causes of dementia

Vascular dementia is a consequence of

cerebrovascular disease

* associated with conditions that cause hypoperfusion in the brain.
* Larger artery disease, cardio embolism, small vessel disease of the brain, stroke

Frontotemporal dementia is

Rare, degenerative disease

Degeneration of frontal and anterior frontal lobes, familial association, most cases involve gene mutation

Seizures is a sudden, transient alteration of the

brain function caused by abnormal excessive discharges of cortical neurons

* manifestation of disease

Convulsion is

tonic-clonic (jerky, contract-relax) movements associated with some seizures

Associated conditions for seizures

metabolic disorders, congenital malformations, genetic predisposition, perinatal injury; postnatal trauma, myoclonic syndromes, infection, brain tumor, vascular disease, substance abuse.

Seizures are classified by

clinical manifestations, site of origin, EEG correlates, response to therapy

Preictal phase of seizures can be

prodroma (hours to days before)

aura ( immediately before)

Ictus is a (seizure episode) but what kind manifestations does it have?

headache, confusion, dysphasia, memory loss, paralysis

Status epilepticus is

state of continuous seizures

Increased intracranial pressure may result from an increase in

intracranial content, cerebral edema, excessive CSF, hemorrhage, tumor growth

Increase in content requires equal reduction, CSF is displaced, cerebral blood volume and flow are altered

Cerebral Edema causes an

increase in the fluid (intracellular or extracellular) within the brain

treatment direct at decreasing IICP

Hydrocephalus is

excess fluid within the cerebral ventricles, subarachnoid space, or both.

Caused by interference in CSF flow, increased fluid production, obstruction within the ventricular system, defective reabsorption

A patient experiences edema in the brain caused by movement of cerebrospinal fluid (CSF) from the ventricles into the extracellular space. What type of edema does this describe?

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Interstitial

Alterations in neuromotor function such as dysfunction in nervous system areas that control movements can cause

alterations in muscle tone, muscle movement, upper and lower motor neuron syndromes, motor neuron disease, amyotrophic lateral sclerosis

Hypotonia and hypertonia is

decreased muscle tone

hypertonia: increased muscle tone

* spasticity, gegenhalten (paratonia), dystonia, rigidity

Hyperkinesia is

excessive, purposeless movement

Paroxysmal dyskinesias

abnormal, involuntary movements that occurs as spasms.

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* involuntary movements: Dystonia (uncontrolled twisting, resulting in abnormal posture)
* chorea (abnormal jerky movements)
* athetosis (slow, irregular, twisting movements most obvious in distal extremities)
* ballism(wild flinging movements of limbs, usually on one side of the body that does not lessen at night)

tardive dyskinesia is

involuntary movement of the face, lip, tongue, trunk, and extremities.

Usually occurs as a side effect of prolonged antipsychotic drug therapy

Huntington disease (Huntington chorea)

autosomal dominant hereditary degenerative hyperkinetic disorder. Rare, hereditary, degenerative hyperkinetic movement disorder. Caused by defect of chromosome 4.

* severe degeneration of the basal ganglia, particularly the caudate nucleus
* Depletion of gamma-aminobutyric acid (GABA)

Hypokinesia is

loss of voluntary movement despite normal consciousness and peripheral nerve and muscle function

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* decreased associated movements accompanying emotional expression cause an expressionless face, statue like posture, absence in speech, locomotion cause reduction in arm and shoulder movements, hip swinging, and rotary motion of the cervical spine

Akinesia

decrease in voluntary and associated movements

Bradykinesia is

slowness of voluntary movements

loss of associated movement

Parkinson disease

severe degeneration of the basal ganglia with loss of dopamine-producing neurons

Hallmark of hypokinesia

Activity in Parkinson are manifested by hypertonia and hypokinesia

Manifestations for Parkinson disease

parkinsonian tremor, rigidity, bradykinesia, postural disturbances, autonomic and neuroendocrine symptoms, cognitive-effective symptoms.

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Stooped posture, short shuffling steps, slow movement poor balance, arms and wrists flexed reduced swing, rigidity,

Upper motor neuron syndromes result of

injury to motor pathways that descend from the motor cortex. upper motor neuron paresis (weakness) or paralysis

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* hemiparesis or hemiplegia, diplegia, paraparesis or paraplegia, quadriparesis or quadriplegia

Lower motor neuron syndromes is the result of

injury to alpha motor neurons and impairs voluntary and involuntary movement.

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Manifestations for Lower motor neuron syndromes

Flaccid paresis/paralysis

Fasiculations

Fibrillation

Motor neuron disease is the result of

progressive degeneration of upper or lower motor neurons.

* Guillain-Barre syndrome, spinal muscular atrophy, progressive bulbar palsy, bulbar palsy

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder which involves

the upper and lower motor neurons

* causes progressive muscle weakness/unknown etiology
* starts with muscle weakness and progresses to muscle atrophy, spasticity, and loss of manual dexterity and gait.

ALS starts with

muscle weakness and progresses to muscle atrophy, spasticity, and loss of manual dexterity and gat,

Fatal from respiratory failure within 3 years of diagnosis

dystonia is the

maintenance of an abnormal posture through muscular contractions. When contraction last for longer periods, they are called dystonic postures.

hypermimesis commonly manifests as pathologic

laughter or crying. pathologic laughter is associated with right hemisphere injury, and pathologic crying is associated with left hemisphere injury.

Basal ganglia motor syndromes is an

imbalance of dopaminergic and cholinergic activity in the corpus striatum

produces hypokinesia and hypertonia

Cerebellar motor syndromes is associated with

ataxia

primarily influence the same side of the body

Traumatic brain injury can be caused by external force like

motor vehicle accidents, falls, unintentional blunt trauma,

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Traumatic brain injury can be primary like

Direct impact, focal (closed or open) or diffuse

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Secondary: indirect consequence of primary injury, systemic and brain tissue responses

Closed brain injury: Grossly observable brain lesions

Head strikes surface or moving object strikes head (motor vehicle accident or falls) (baseball or falling objects)

* the dura remains intact and brain tissues are not exposed to the environment

Location of injury in closed brain injury

coup- injury directly below point of impact

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Countercoup- injury OPPOSITE the site of impact

Injuries for closed brain injury include

contusions, subdural or epidural hematomas, intracerebral hemorrhage

Open brain injury is an injury that breaks

the dura and exposes the cranial contents to the environment. __**Occurs with penetrating trauma or skull fracture**__

* causes both focal and diffuse injuries
* compound skull fracture
* missile injuries

Diffuse brain injury(DAI) involves

widespread areas of the brain. Coma lasting 6-24 hours after TBI. Acceleration/ deceleration or rational forces cause axonal damage.

* shearing, tearing, or stretching of nerve fibers

severity corresponds to the amount of shearing force applied to the brain stem

Secondary brain injury is an indirect result of primary brain injury. Systemic processes for this injury include

hypotension, hypoxia, anemia, hypercapnia, hypocapnia.

Cerebral processes: inflammation, cerebral edema, increased intracranial pressure, decreased cerebral perfusion pressure, cerebral ischemia, brain herniation

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Prevention of hypoxia and maintenance of cerebral perfusion pressure

Categories of mild TBI (mild concussion) is

none or short loss of consciousness

confusion for several minutes, retrograde amnesia

Moderate TBI (moderate concussion)

loss of consciousness 30 minutes to 6 hours

confusion with amnesia longer than 24 hours

severe TBI (severe concussion)

loss of consciousness longer than 6 hours

severe cognitive system defects

Complications of TBI Like post concussion syndrome lasts for

weeks or months post mild concussion

symptomatic relief with observation

Posttraumatic seizures occur within

days, last up to 2-5 years post injury

seizure prevention initiated early with moderate to severe TBI

Chronic traumatic encephalopathy is a

progressive dementing disease from repeated injury,

* sports injuries, blast trauma, work-related head trauma

Violent behaviors, loss of control, depression, memory loss, change in cognition and motor function

Primary spinal cord injury occurs with

initial mechanical trauma and immediate tissue destruction

* inadequate mobilization following injury
* may occur in absence of vertebral fracture or dislocation

Secondary spinal cord injury is a pathophysiologic cascade of events that begins

immediately after injury and continues for weeks.

* hemorrhages, inflammation, edema, ischemia

Life threatening if swelling occurs in cervical region

* cardiovascular and respiratory control can be lost

vertebral injuries result from

acceleration, deceleration, or deformation forces

Spinal shock is

normal activity of the spinal cord ceases at and below the level of injury; sites lack continuous nervous discharges from the brain.

Spinal shock has complete loss of reflex function and

flaccid paralysis, absence of sensation, loss of bladder/ rectal control, transient drop in blood pressure, bradycardia, poor venous circulation

In Autonomic hyperreflexia, sensory receptors below the level of the cord lesion are stimulated. The intact autonomic nervous system responds with

an arteriolar spasm that increases blood pressure. Baroreceptors in the cerebral vessels, carotid sinus, and aorta sense hypertension and stimulate the prismatic system. HR decrease, visceral and peripheral vessels don’t dilate because impulses cannot pass through cord

Symptoms for autonomic hyperreflexia include

paroxysmal hypertension (300 systolic), a pounding headache, blurred vision, sweating above level of lesion, flushing of the skin, nasal congestion, nausea, bradycardia

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Can cause serious complications: stroke, seizures, myocardial ischemia, and death

The most common cause for autonomic hyperreflexia is

distended bladder or rectum; sensory stimulation (skin or pain receptors) can elicit autonomic hyperreflexia

Spasticity

A gradual increase in tone causing increased resistance until tone suddenly diminishes

Paratonia

resistance to passive movement

dystonia

sustained involuntary muscle contraction with twisting movement as shown on the picture

rigidity

muscle resistance to passive movement of a rigid limb that is uniform in both flexion and extension throughout the motion

Most common symptoms for tardive dyskinesia are

rapid, repetitive, stereotypic movements, such as continual chewing with intermittent protrusions of the tongue, lip smacking, and facial grimacing.

Tourette syndrome is the hallmark of TS which is the presence of

Motor tics and vocal tic.

symptoms of huntington disease include

progression slowly over 15-20 years. extrapyramidal and include involuntary hyperkinetic movements, chorea, athetosis, and ballism.

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Cognitive deficits: slow thinking, loss of working memory, reduced capacity to plan, organize, and sequence. restlessness, disinhibition, and irritability. apathy, depression, anxiety

Dystonic postures last for

weeks, causing permanent, fixed contractures

Basal ganglion posture refers to

stooped, hyperflexed posture with a narrow based, short stepped gait

Hypomimesis manifests as

aprosody- the loss of emotional languae: receptive or expressive aprosody