More Disorders Of The Nervous System

Front 1

What is diffuse brain injury?

Back 1

It's due to rotational or acceleration-deceleration movement injuries
Can shear blood vessels and neural tissue
Major effect is diffuse axonal injury resulting in swelling of the neuronal axons and oligodendorcytes
Damage ranges from mild to severe depending on degree of consiousness and recocery of funcion
5 classifications: Mild concussion, classic cerebral concussion, Mild diffuse brain injury, moderate diffuse brain injury, severe diffuse brain injury

Front 2

Mid concussion

Back 2

causes confusion and memory loss; usually no loss of consciousness, full recovery of all neural function generally occurs

Front 3

Classic cerebral concussion

Back 3

causes loss of consciousness for less than 6 hours, a full recovery of all neural function should occur

Front 4

Mild diffuse brain injury

Back 4

Induces coma for up to 24 hours although a full recovery is expected. Some small, lingering neural deficits may persist

Front 5

Moderate diffuse brain injury

Back 5

Induces coma for over 24 hours; death can result, permanent brain damage

Front 6

Severe diffuse brain injury

Back 6

Induses a prolonged coma, death frequently results

Front 7

What is the cause and pathogenisis of cerebral infraction?

Back 7

Loss of blood supply to an area of the brain due to vascular occlusion, the ischemia initiates teh pathogenesis of the rtrok resulting:
1. Cell death
2. Injured cells-neurons display axonal degeneration while the oligodendrocytes show myelin degeneration
3. Membrane permeability is increases
4. Ca influx slows enzymes of aerobic respiration resuliting in a decrease of ATP to run the Na-K pump as Na accumulates inside the cell with H2O leading to cellular edema
5. Glutamate release from the injured cells makes the membrane more permeable to Na and K. H2O osmotically follows solute into the cell causing cytotoxic (cellular) edema
6. Ischemia further depresses aerobic respiration; with a drop in ATP production, increased levels of lactic acid is produced, resulting drop in blood pH

Front 8

What is the ethiology of cerebral hemorrhage?

Back 8

Hypertension and necrosis cause small arteries to rupture
Hemorrhage results in vasogenic edema
Increase in fluid of the interstitial fluid space compresses the surrounding tissue
The Compuression and vasogenic edema increases intracranial pressure
Increased pressure is exerted on all nervous tissue in the brain resulting in a hyperirritability

Front 9

What are the main mainfestations of cerebral hemorrhage which may or may not be reversible?

Back 9

1. Sensory: contralateral loss of general sensations including proprioception; general senses of touch, temp, pain, and proprioception are diminished.
2. hemianopsia, quadrantanopsia, mydrisis, diplopia, opthalmoplegia

Front 10

What are the motor function signs/symptoms of cerebral hemorrhage? (10)

Back 10

1. Contralateral hemiparesis or hemiplegia
2. Apraxia-loss of ability to carry out familiar movements
3. Contralateral hyperhidrosis-sweating on one side of the body
4. Dysarthria-imperfect articulation of speech
5. Aphasia-difficulty speaking more than several words due to damage to Broca's area
6. Akinetic mutism-due to destruction of the motor speech area
7. Dysphagia
8. Dysmetria-difficulty estimating range of motion
9.Cerebellar ataxia, tremor, and palsy
10. Damage to teh cerebellum-results in muscle incoordination, quivering, and paralysis

Front 11

What are the cognitive signs/symptoms of cerebral hemorrhage? (4)

Back 11

1. Anomia-inability ot recognize objects
2. Prosopagnosia-inability or recognize familiar faces
3. Decreased alertness, LOC, coma
4. Damage to subcortical structures-decreased awareness, semiconsciousness, coma

Front 12

What is the main autonomic function sign that manifests with cerebral hemorrhage?

Back 12

Cheyne-Stokes respirations which manifests as difficult, labored breathing.

Front 13

How are seizures defined?

Back 13

A sudden, abnormal increase in electrical impulses within the brain

Alteraations in motor function, sensory detection, autonomic control, and cognition

Front 14

What is the etiology of seizures?

Back 14

1. Epilepsy: idiopathic, triggered by multitude of factors including psychological, environmental, genetics
2. Brain trauma: accidents
3. Brain lesions: tumors
4. Biochemical disorders: drug overdose
5. Functional: psychological

Front 15

What are generalized seizures?

Back 15

They occur simultaneously in different locations throughout the brain; origin is always in the deeper areas of the cerebral cortex and occurs in both hemispheres of the brain
Different types:
Absence (petit mal)
Clonic
Tonic
Infantile spasms
Atonic
Tonic-clonic

Front 16

Absence (pitit mal) seizures

Back 16

person stres for a few seconds and temporarily disconnects from their environment

Front 17

Clonic Seizures

Back 17

Repetitive contractions and relaxation

Front 18

Tonic seizure

Back 18

Loss of muscle tone in back (postural tone); increased muscle tone in the limbs result in arms flexion and extension in the legs; occurs in infants and children

Front 19

Infantile spasms

Back 19

Occur in infants where the head adn limbs flex into a jackknife position; in half of these cases this is a manifestation of another disorder

Front 20

Atonic seizures

Back 20

Characterized by a sudden loss of postural tone; this can manifest as a mild head nod to the extreme of falling down hard.

Front 21

Tonic-clonic (grand mal) seizures

Back 21

Patient usually experiences and aura or prodrome, then falls unconscious; strong tonic phase with apnea followed by a clonic phase characterized by violent contraction and subsequent relaxation periods; terminal phase of no movement occurs just prior to regaining consciousness

Front 22

What are status epileptics?

Back 22

Continuous, severe seizures
A 250% increase in ATP consumption
Although cerebral blood flow increases to meet this demand, nutrients and particularly oxygen are rapidly depleted
Lactic acid levels rise
Metabolic acidosis and hypoxia initially cause neuronal exhaustion
Neurons could be destroyed due to the lack of O2
Simultaneous hypermetabolism and ischemia accompanying numerous seizures can result in brain death

Front 23

What is the etiology of multiple sclerosis?

Back 23

Chronic degeneration of myelin sheaths

An autoimmune disoreder; T cells attack a specific protein in myelin which can be triggered by a previous viral infection

There appears to be a genetic predisposition

Glosis: as demyelination progresses, plaque or aggregates of affected myelin appear

Inflammatory edema: Gluosis induces inflammation of the neurons within the affected myelin sheaths. This inflammation leads to edema

Front 24

What are the 4 distinct syndromes of multiple sclerosis?

Back 24

1. Brain stem effects: involve CNII, demyelination leads to optic neuritis and visual deficits; NC VIII demyelination leads to vertigo and nausea; dysarthia also results
2. Cerebellum: affects involuntary control of movement; manifests as motor ataxia; other manifestations include hypotonia, lowered muscle tone, and asthenia
3. Spinal cord: affects both motor and sensory tracts; spastic ataxia, bladder and bowel function is also adversely affected. Sensory alterations in limbs
4. Cognition: manifests as memory loss, lack of concentration, and mood alterations

Front 25

What is the etiology of Amyotrophic lateral sclerosis (ALS)?

Back 25

CAuse is idiopathic but ther eis a genetic link

Scarring of the motor nerves and associated muscle wasting with disuse

40-50 yrs

Defective chromosome 21 results in an ineffective superoxide dismutase enzyme that normally destroys free radicals suggesting that the cause of ALS is due to high levels of free radicals

Might also be triggered by a viral infection

Front 26

What happens in ALS patients?

Back 26

Progressive asymmetic muscle weakness

the axons of motor neurons degenerate

Glial proliferation results in secondary demyelination

Degeneration of upper motor neurons results in "lateral sclerosis"

Degeneration of lower motor neurons results in "amyotrophy"

Eventually the muscles of breathing are involved resulting in death

Front 27

Alzheimer's

Back 27

~Degeneration of cerebral cortex-result in altered cognition and behavioral changes associated with disease

~Appears in individuals over 65

~Progression to complete dementia within 8yers

~Idiopathic-genetic component

~Abnormalities in chromosome 14 or 21 are common

~Repeated head trauma is correlated with disease

~Atrophy of gyri of cerebral cortex causes increased depth of sulci

~Amyloid plaque: abnormal beta amyloid protein which is deposited in the extracellular spaces resulting in neuritis and amyloid angiopathy

~Neurofibrillary tangles: abnormal tau protein from the microtubules from neurofibruillary tangles within the axon resulting in decreased neurotransmitter transport and altered action potential conduction

~Neurotransmitter changes: decreased synthesis of neurotransmitters resulting in decreased levels of acetylcholine, somatosin, substance P

Front 28

What are the clinical manifestations of Alzheimer's Disease?

Back 28

~Mental changes: including nocturnal awakenings

~Physical changes: weight loss from muscle disuse, loss of coordination, bladder/bowel function

~Death: frequently choke on saliva or food leading to asphyxiation; infection from aspiration pneumonia is another frequent cause of death; accidents

Front 29

What is the etiology of Parkinson's Disease?

Back 29

~Degeneration of dopamine secreting neurons of substania nigra of the basal ganglia

~Med age=60; as early as 40

~More prevalent in men

~Idiopathic

~Secondary form can be caused by overdose on designer drugs, manganese dust, carbon monoxide poisoning, and severe head trauma

~Certain prescribeddrugs cause a reversible Parkinson-like syndrome including neurolepics, antiemetics, and antihypertensives

Front 30

What are the manifestations of Parkinson's Disease?

Back 30

~Basal ganglia, primarily the substantia nigra (that secretes dopamine) degenerates possible due to oxidative stress

~Decreased dopamine levels

~Limbic system and diencephalon are affected; neurons in the areas secrete serotonin, thus, decreased serotonin production

~Cerebral cortex is also affected in some individuals leading to cerebral atrophy and neuronal loss

~Neurotransmitter imbalance: excitatory acetylcholine favored over dopamine with is inhibitory

Front 31

What motor impairment is associated with Parkinson's Disease?

Back 31

1. Akinesia: loss of movement, hypokinesia (sitting abnormally still), and bradykinesia (slow movement)
2. Hypertonia: abnormal muscle tone manifests as hand and foot tremors; tremors increase with stress adn anxiety but decrease during purposeful movement and sleep; muscle rigidity or abnormal contraction
3.Posture: altered, manifests as stooped shoulders; loss of equilibrium resulting in tilt
4. Final motor progression: decreased facial expression and drooling; a slow, shor, shuffling gate
5. Neuroendocrine effects: a slowed autonomic nervous system resulting in diaphorsis, orthostatic hypotension, gastric retention, constipation, and urinart retention; seborrhea or oily skin also appears
~Depression in 50% and dementia in 30%

Front 32

What is the ethiology of meningitis?

Back 32

~Infection of the meningers, particularly the pia matter and arachnoid
~Bacterial meningitis is the most common
~Can occur by a blood-borne pathogen crossing the choroid plexus into the CSF
~Severe trauma causing a break in the dura mater allows direct contact of bacteria with CSF
~Bacterial infections of the mouth, sinuses or middle ear travel by cranial or peripheral nerves into the subarachnoid space
~Aseptic meningitis refers to viral infection
~Inflammation extends into cranial/peripheral nerves
~Neutrophils attack the microorganisms in the subarachnoid space resulting dead microorganisms called exudates that thickens teh CSF
~Ventricular system is blocked increasing the amount of SCF and swelling the ventricular system
~The increased CSF causes edema of the meninges disrupting cell membranes

Front 33

What are the signs of meningitis?

Back 33

Headache
vomiting
nuchal rigidity (still neck)
Kernig sign (contraction/pain of the hamstring muscles during extension of the leg after flexing the thigh

Front 34

What are the neural manifestations occurring in meningitis?

Back 34

~Decreased LOC: from pressure on the reticular activating system
~Cranial/peripheral nerve palsies: papilledema is blindenss caused by pressure on CNII; disturbances such as ptosis (drooping eye) and diplopia (double vision) result from pressure on CNIII, IV, and VI; CNV causes photophobia (sensitivity to light
~Facial paresis from pressure on CN VII
~Deafness, tinnitus, and vertigo result from pressure on CN VIII