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Most common sign of brain dysfunction
altered level of consciousness and change in behavior .
Levels of Consciousness: reflect orientation to person, place, and time
• Consciousness, confusion, delirium, obtundation, stupor, coma • Glascow Coma Scale
Posthyperventilation apnea (PHVA)
resp stop after hyperventilation has lowered Pco2 level below normal
Cheyne-Stokes respirations (CSR):
breathe-> apnea-> inc. RR & depth-> gradual decease to point of apnea
Pupillary Reflexes and Eye Movements
– Pupils become unreactive and dilated as brain function deteriorates
– Bilateral loss of pupil response indicates brain stem problems
– Unilateral response indicates optic (II) or oculomotor (III, IV, VI) problem
– Doll’s eyes: eyes roll opposite of way head moves
– Flexion of arms, wrists, fingers, adduction of upper extremities, internal rotation, plantar flexion of feet (fig. 14-6A)
– Results from lesions of cerebral hemisphere or internal capsule (above midbrain)
– Rigid arms with palms turned away from body, stiffly extended legs with plantar extension of feet (fig. 14-6B)
– Lesions of diencephalon extend into midbrain and upper brain stem.
Coma is produced by either:
– Bilateral hemisphere damage or suppression
– Brain stem lesions or metabolic derangement that damages or suppresses the reticular
Total Brain Death:
irreversible loss of function of the brain, including brain stem
loss of all cognitive functions (injury affecting cerebral cortex)
and the unawareness of self and surroundings for at least one month.
Provoked (secondary, acute symptomatic)
– Febrile seizures: fever > 104
– OR Precipitated by metabolic conditions: electrolytes imbalances, hypoglycemia, hypoxia,
uremia, CNS infections, etc.
– OR Following a primary insult to CNS
• Unprovoked (primary, idiopathic) – No identifiable cause known
Sudden, transient alteration of brain function caused by an abrupt explosive, disorderly discharge of cerebral neurons
Motor, sensory, autonomic, or cognitive effects
a term sometimes applied to seizures refers to clonic-tonic (jerky, contract- relax) movements associated with some seizures
seizure activity with no underlying correctable cause; seizure activity recurs
involve only one hemisphere; not accompanied by loss of consciousness. Can have motor, sensory and autonomic signs and symptoms.
• depends upon area of brain involved
– Impairment of consciousness and often arise from temporal lobe
– May or may not be accompanied by automatisms:
• Repetitive, nonpurposeful activity such as lip smacking, grimacing, patting, or rubbing clothing
– Confusion during postictal state (recovery time that follows the seizure)
begin with involvement in both hemispheres
generalized, nonconvulsive epileptic events expressed mainly as disturbances in consciousness
• Blank stare, motionless, unresponsiveness, automatisms, changes in postural tone
*Manifestations so subtle they may go unnoticed.
– Aura or Prodroma
Then sharp contraction of muscles with extension of extremities and immediate loss of
consciousness. Incontinence is common
3. Postictal period.
sudden, split-second loss of muscle tone leading to slackening of jaw, drooping of limbs, or falling to the ground. “Drop attacks”
H&P, neuro exam, full account of seizure activity, labs to rule out metabolic problem, CT/MRI, EEG (brain electrical activity)
Meds, surgery if refractory to drug therapy
– Experience of a second seizure before the person has fully regained consciousness from the preceding seizure or a single seizure lasting more than 30 minutes
– Seizures that do not stop spontaneously or occur in succession without recovery.
– If seizure activity is not broken, could lead to respiratory failure.
a syndrome of intellectual deterioration severe enough to interfere with occupational or social performance.
Manifested by loss of recent and remote memory
Progressive failure of cerebral functions that is not caused by an impaired level of
Alzheimer’s Disease (Cortical Dementia)
50-70% of all cases of dementia
-Caused by gene mutations (APOE-e4), Down’s syndrome (early onset), familial
--Cortical atrophy and loss of neurons, particularly in parietal and temporal lobes
--Decrease in choline acetyltransferase, an enzyme required for memory function results in the presence of amyloid-containing senile plaques and neurofibrillary tangles.
(proteins in neuron become twisted & distorted) are resistant to chemical breakdown and are present long after the neuron disappears.
--seen in alzheimers patients
The number and distribution of senile plaques (plaque-like material that disrupts nerve-
impulses transmission) determines the severity of the dementia
– Forgetfulness, emotional upset, disorientation, confusion, lack of concentration, decline in abstraction, problem solving, and judgment
– Follows an insidious and progressive course
short-term memory loss (randomly forget important and unimportant information) and denial of such memory loss, subtle personality changes [social withdrawal, lack of spontaneity])
Confusional stage (stage 2) Alzheimer's
(several years): global impairments of cognitive functioning (language, spatial relationships, problem solving), depression, confusion, disorientation, unable to do ADL’s, wandering, “sundown syndrome” in late afternoon, hostile/abusive toward family members,
incontinent, apathetic, unable to recognize family
diagnosis of exclusion-rule out other causes of dementia, Hx including mental status exam and course of illness; Gene tests
no cure available, maintain person’s socialization and provide support for family; Drugs may be able to slow the disease process, and Aricept had modest effect on cognitive function
Can obstruct cerebral blood flow, destroy brain cells, displace brain tissue (volume)
Normal ICP: 5-15 mm Hg
Brain tissue (80%)
Small increases in cranial vault causes:
contents can be compensated for by decreasing another component.
Brain tissue- relatively constant (least able to compensate)
Cerebral Perfusion Pressure (CPP)
pressure to get blood to brain and into brain tissue
– Difference between mean arterial pressure and the ICP(MAP – ICP = CPP); pressure perfusing the brain.
Normal: 70-100 mmHg
Problems occur when ICP nears or exceeds MAP results in dec. CPP and result in brain tissue hypoxia
– Caused by an increase in intracranial content
•Tumor growth, edema, excessive CSF, or hemorrhage in brain tissue
impaired O2 delivery: reduced atmospheric pressure, CO poisoning, severe anemia, failure to oxygenate blood.
(impaired delivery of O2 & glucose & removal of metabolic wastes): focal (single area of brain) or global [entire brain-no collateral circulation, unconsciousness within seconds]
Excitatory Amino Acid Injury
• Glutamate – principal excitatory neurotransmitter
•During injury, extracellular glutamate cannot get into the cells and accumulates.
increase in tissue volume secondary to abnormal fluid accumulation (intracellular or extracellular) within brain tissue
results from increase in the ECF that surrounds the brain cells (tumors, prolonged ischemia, hemorrhage, brain injury, infections)-blood brain barrier is disrupted
swelling of brain cells (hypo-osmotic states [impairs Na-K pump= inc. intracellular fluid] – water intoxication, severe ischemia)
Both components of vasogenic & cytotoxic edema. Follows cerebral infarction. Brain cells become necrotic & die-release lysosomes=inc. blood brain permeability
CSF moves into extracellular spaces of brain tissues from ventricles. Noncommunicating hydrocephalus
Progressive degenerative disorder of basal ganglia resulting in degeneration of the dopamine nigrostriatal system.
regulates the overall excitability of the striatum
may play role in early onset Parkinson’s (<45 years). Usual onset >50yrs (58-62 yrs of age)
Lewy dementia is seen in about 20% of cases. Postural disturbance
Tremor at rest– usually affects hands/feet, head and neck areas; disappears with movement
--Muscle Rigidity – resistance to movement of both flexors and extensors throughout full ROM; takes considerable energy to move; jerky
--Slowness of movement (bradykinesia) – slowness in initiating and performing movements and difficulty in sudden, unexpected stopping of voluntary movements.
must be individualized, nonpharm. (diet & exercise), pharm, surgery
– A traumatic insult to the brain possibly producing physical, intellectual, emotional, social,
and vocational changes
– Head injury is leading cause of death in US among persons younger than 24 years.
– 50% are motor vehicle accidents
– 21% are falls
– Others: violence and sports
Open (penetrating, missile) trauma
– Injury breaks the dura and exposes the cranial contents to the environment
– Causes primarily focal injuries
Blunt (closed, nonmissile) trauma
– Head strikes hard surface or a rapidly moving object strikes the head
– The dura remains intact and brain tissues are not exposed to the environment
– Causes focal (local) or diffuse (general) brain injuries
• Coup-contrecoup injury – brain moves back and forth after impact
• Coup injury- Injury directly below the point of impact
• Contrecoup- Injury on the pole opposite the site of impact
• Smaller area of impact-inc. severity of injury because force is concentrated into smaller area.
– Bruise (contusion) to the cortical surface of the brain caused by blunt trauma (like head hits windshield)
– Generally result of anteroposterior displacement when head strikes fixed object
– Brain tissues are bruised and torn; can cause damage to brain tissue forming scar tissue
– Extradural (epidural) hemorrhages or hematomas
– Subdural hematomas
– Intracerebral hematomas
result from vascular injury and bleeding
develops between the bones of the skull and the dura
-Usually a tear in the middle meningeal artery in temporal area
– Rapid compression of brain occurs
– Head injury with brief period of unconsciousness followed by lucid period followed by rapid progression to unconsciousness again
develops in area between the dura and subdural space
– Usually result of tearing in veins so subdural hematoma developing slower
• Acute: symptoms seen within 24 hours
• Subacute: symptoms within 2-10 days after injury
• Chronic: symptoms after several weeks
– Most common type of traumatic brain injury
– Temporary axonal disturbances causing momentary attention and memory deficits but no
loss of consciousness
• Recovery usually occurs in 24 hours
•Headache, irritability, insomnia, poor concentration and memory may last for months
– I—confusion, disorientation, and momentary amnesia
– II—momentary confusion and retrograde amnesia after 5-10 min.
– III—confusion with retrograde (amnesia for events preceding trauma) and anterograde
(can’t form new memories) amnesia
– Diffuse microscopic damage to axons in cerebral hemisphere, corpus collasum, and brain stem
– Disconnection of cerebral systems from the brain stem and reticular activating system
– Physiologic and neurologic dysfunction without substantial anatomic disruption
– Immediate loss of consciousness (up to 6 hours)
– Anterograde and retrograde amnesia
Most commonly occurs due to vertebral injuries
– Simple fracture, compressed fracture, and comminuted fracture
cervical (1-2, 4-7), and T10–L2 lumbar vertebrae
Locations reflect most mobile portions of vertebral column and the locations where the
spinal cord occupies most of the vertebral canal
Complete Spinal Cord Injury (def. & Tx)
Absence of motor and sensory function below the level of injury
reduce neurologic deficit and prevent any loss of further neuro function
– Normal activity of the spinal cord ceases at and below the level of injury. Sites lack continuous nervous discharges from the brain.
– Flaccid paralysis with transient loss of somatic control and autonomic reflexes below level of injury, absence of somatic and visceral sensations, loss of bowel/bladder function, reflex function
– Transient nature of spinal shock related to accumulation of edema within the spinal cord
CO2, H+, and O2 affect on cerebral flow
• Increased CO2 and H+ increase cerebral blood flow (vasodilation) • Decreased O2 increases cerebral blood flow (vasodilation)
Cerebrovascular disease (CVD)
any brain abnormality caused by a pathologic process in the blood vessels either ischemia or hemorrhage. (Stroke)
(Brain attack, CVA, Stroke syndromes): is the clinical manifestation of CVD.
Acute nonconvulsive focal neurologic deficit resulting from a vascular disorder that injures brain tissue.
Age (>65), gender (men), race (Black), heart disease, HTN, high cholesterol, smoking, prior stroke, diabetes, dehydration
caused by interruption of blood flow in a cerebral vessel with or without infarct (70-80% of strokes)
Thrombi (Large vessel) Stroke
– atheroscleosis plaque of carotid arteries
• Cerebral atherosclerosis at bifurcation of artery (internal carotid & vertebral arteries or junctions of basal and vertebral arteries).
–Aphasia, hemineglect syndrome, visual field deficits, transient blindness
Caused by primarily cardiac conditions in left heart (blood goes straight to brain)
–Rheumatic heart disease, atrial fib, MI, ventricular aneurysm, bacterial endocarditis
–Sudden onset with immediate maximum deficit
Small cerebral infarcts located in deeper areas of brain or brain stem in smaller branches of the arteries
• Associated with smoking, hypertension, DM
• May have pure motor hemiplegia, pure sensory hemiplegia
Transient Ischemic Attacks (TIA)
– Subcategory of thrombic strokes
– Focal ischemic cerebral neuro deficit that last from few minutes to 1-2 hours such as weakness of upper & lower extremities on one side; no infarction
– Equivalent to “brain angina” – temporary disturbance in focal cerebral blood flow
– *Warning sign of impending stroke-increasing frequency or longer duration
– S&S depend upon artery involved; always sudden in onset and focal and usually one-
– Most common symptom: unilateral weakness of face, arm, or leg (less common)
– Other S&S: unilateral numbness, vision loss, language disturbance (aphasia) slurred
speech, loss of balance
H&P, neuro exam, CT/MRI, arteriography, ultrasounds/dopplers
thrombolytics (major risk of bleeding), educate public to seek treatment without delay
Infection spreads via CSF that bathes brain and spinal
resistance to extension of the leg while person is lying with hip flexed at a right angle-inc. pain
person has Meningitis
Lumbar puncture: cloudy, purulent CSF (high neutrophils, increased protein count, reduced sugar content
antibiotics; vaccinations for meningococcal, pneumococcal
– Course is less severe than bacterial
– CSF: lymphocytes and normal sugar content
- RX symptomatic (let it run course); may use antiviral and steriods
– Acute febrile illness, usually of viral origin with nervous system involvement; but could be other organisms
– Most common forms of encephalitis are caused by arthropod-borne viruses and herpes simplex virus– Localized necrotizing hemorrhage with edema
Multiple Sclerosis is an autoimmune progressive, inflammatory, axional demyelinating disorder of the CNS nerve fibers that spares the PNS.
(ranging from decreased. conduction velocity to conduction blocks) of nerve fibers in white matter of brain, spinal cord, and optic nerve.
Hard, sharp-edged patches (plaques) appear in white matter and diffuse lesions (periventricular demyelination) result from an immune-mediated inflammatory response to a virus in genetically susceptible people.
Relapsing-remitting (90%); Secondary progressive; Primary progressive; Progressive
hypercalcemia, fever, emotional stress
CSF analysis (elevated IgG levels), MRI
Modify course of disease (diet, rest, exercise, avoid fatigue, stress, infections), meds
• Neuromuscular junction serves as a synapse between a motor neuron and a skeletal muscle fiber .
Acetylcholine (ach) is required for muscle contraction and inactivated by acetylcholinesterase enzyme which allows repeated muscle contractions and gradations of contractile force.
May progress to respiratory muscle weakness, chewing/swallowing may be difficult; even with sustained effort.
muscle weakness is severe enough to cause respiratory problems
H&P, anti-acetylcholinesterase test, steroids, plasmaphoresis, thymectomy
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