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Neurological Pathophysiology

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Title: Neurological Pathophysiology


1
Neurological Pathophysiology
2
Edema in the CNS
  • Increase in tissue mass that results from the
    excess movement of body fluid from the vascular
    compartment or its abnormal retention in the
    tissue.
  • Why is this a special problem in the brain and
    spinal cord?
  • Enclosed space
  • Lack of lymphatics
  • Lack of anastomoses in venous drainage

3
Vasogenic edema
  • Occurs when the blood-brain barrier is upset
  • Inflammation due to infection
  • Toxic agents that damage capillary endothelium
  • Abnormal capillaries associated with malignant
    neoplasm
  • Leakage of proteins fluid into interstitium ?
    swelling
  • Plasma filtrate accumulation alters ionic balance
    and impairs function

4
Cytotoxic edema
  • Intracellular phenomenon
  • Hypoxia
  • Cardiac arrest
  • Near drowning
  • Strangulation
  • Focal edema due to blockage of an end artery
  • Toxic substances that
  • Impair sodium/potassium pump
  • Impair production of ATP

5
  • In practice, swelling often caused by both
  • Treatment is different
  • If swelling is due to cytotoxicity, can give I.V.
    bolus of a hypertonic solution such as mannitol
    to draw water into the vasculature and out of the
    brain
  • If the cause is vasogenic would this help?
  • No! would draw fluid into interstitial space and
    increase swelling!!

6
Increased intracranial pressure (IICP)
  • Normal intracranial pressure is 5-15 mm Hg
  • May be due to
  • Tumor growth
  • Edema
  • Excess cerebrospinal fluid
  • Hemorrhage

7
Contents of cranium
  • Tissue of the Central Nervous System
  • Cerebrospinal Fluid (CSF)
  • Blood
  • An increase in any one of these increases
    intracranial pressure.
  • Clinical hallmarks of IICP
  • Headache
  • Vomiting
  • Papilledema swelling of the optic discs

8
  • Since the brain is encased in the cranium, the
    only way pressure can be relieved is by
    decreasing cranial contents.
  • Most readily displaced is CSF
  • If ICP still high, cerebral blood volume is
    altered
  • Stage 1 vasoconstriction and external
    compression of the venous system
  • Compensating, so few symptoms

9
  • If ICP continues to increase, may exceed brains
    ability to adjust.
  • Stage 2
  • IICP (gradually rising) causes a decrease of
    oxygenation of neural tissue
  • Systemic vasoconstriction occurs to increase
    blood pressure to get blood to brain
  • Clinical manifestations transient episodes of
    confusion, restlessness, drowsiness, and slight
    pupillary and breathing changes

10
  • When ICP begins to arterial pressure, there is
    a lack of compensation- beginning decompensation
  • Stage 3
  • Hypoxia and hypercapnia ? cytotoxic edema
  • Decreasing levels of arousal
  • Widened pulse pressure
  • May begin Cheynes-Stokes respirations
  • Bradycardia due to increased pressure in
    carotid arteries
  • Pupils small and sluggish
  • Surgical or medical intervention needed

11
  • When all compensatory mechanisms have been
    exhausted
  • Stage 4
  • Dramatic rise in ICP in a short time
  • Autoregulation is lost, and get vasodilation,
    further increasing intracranial volume
  • ? cerebral perfusion severe hypoxia and
    acidosis
  • Brain contents shift (herniate) from area of high
    pressure to areas of lower pressure ? blood flow

12
  • Small hemorrhages develop
  • Ipsilateral pupil dilation and fixation,
    progressing to bilateral fixed and dilated pupils
  • When mean systolic arterial pressure equal ICP,
    cerebral blood flow ceases

13
Treatment
  • Remove the cause of the IICP
  • Mechanical hyperventilation to medicated and
    comatose patient
  • Reduce blood pressure through diuretics, which
    slows production of CSF and decreases blood-brain
    volume
  • Drugs, us. Barbiturates to slow brain metabolism
    and ? effects of hypoxia
  • Emergency craniotomy to relieve pressure

14
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15
Brain Trauma
  • Highest risk
  • 15 to 30 years of age
  • Infants 6 mo. to two years
  • Young school age children
  • Elderly persons
  • Male female 31

16
  • Most likely causes of head injury
  • Transportation accidents
  • Falls
  • Sports related events
  • Violence

17
Two major categories of head trauma closed
(blunt) trauma open (penetrating) trauma
18
Open (penetrating) trauma
Break in dura results in exposure of brain
tissues to environment. Results in focal
(localized) injury May be due to skull fracture
or wound intracerebral hematoma Traumatic
pneumocephalus - injury to a nasal sinus that
allows air into brain or ventricles -
cerebrospinal rhinorrhea
19
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20
Blunt Head Trauma
More common than open trauma. Involves head
hitting hard surface or rapidly moving object
strikes head Dura is intact no brain tissue
exposed May cause focal or diffuse axonal injury
(DAI)
21
Serious injury decrease due to Seat belt
use Improved management
22
Mild cerebral concussion
  • 75- 90 of all head injuries
  • Not severe
  • Diffuse axonal injury no visible signs on brain
  • May see transient dizziness, paralysis,
    unconsciousness, unequal pupils and shock.
  • Reactive period vomiting, Temp 99 -100o, rapid
    pulse, headache, and cerebral irritation lasting
    12 -24 hours.

23
Contusions (bruise) impacts which lead to
hemorrhage and possibly hematoma Coup (strike)
head strikes against object shearing forces
cause small tears in blood vessels (subdural
vessels) edema severity force smaller area
greater force
24
Contrecoup (rebound) brain hits opposite side
of skull shearing forces and damage opposite to
site of impact
25
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26
Extradural (Epidural) Hematomas
  • 1-2 of major head injuries
  • Most common in 20-40 year olds
  • Often caused by temporal skull fracture or
    injury
  • Artery is often the source of bleeding
  • Get herniation (shift) of temporal lobe of brain
    through tentorial notch

27
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28
Subdural hematomas
  • 10 - 20 of persons with traumatic brain injury
  • Develop rapidly (within hours)
  • Typically on top of skull
  • Often due to tearing of veins or dural sinuses
  • Acts as an expanding mass ? IICP? herniation of
    brain

29
Intracerebral hematomas
  • 2-3 of head injuries
  • Single or multiple
  • Usually frontal and temporal lobes
  • May occur in deep white matter
  • Small blood vessels injured by shearing forces
  • Acts as expanding mass, compresses tissue, and
    causes edema
  • May appear 3- 10 days after head injury

30
Clinical manifestations of contusions
  • Loss of consciousness, loss of reflexes
  • Transient cessation of breathing
  • Brief bradycardia
  • Decreased blood pressure
  • As hematoma enlarges
  • headache, vomiting, drowsiness, confusion,
    seizure, hemiparesis

31
Treatment
  • Contusions
  • Control intracranial pressure
  • Drugs can relieve fluid pressures may alter Na
    conc. in brain fluids
  • Manage symptoms
  • hematomas
  • Surgical ligation

32
Cerebrovascular Disease
  • Most frequent of all neurological problems
  • Due to blood vessel pathology
  • Lesions on walls of vessels leading to brain
  • Occlusions of vessel lumen by thrombus or embolus
  • Vessel rupture
  • Alterations of blood quality

33
CV disease leads to two types of brain
abnormalities Ischemia (with or without
infarct) Hemorrhage
34
Cerebrovascular Accident (Stroke)
  • Clinical expression of cerebrovascular disease a
    sudden, nonconvulsive focal neurological deficit
  • Incidence third leading cause of death in U.S.
    half a million people a year one third will die
    from it

35
Incidence
  • Highest risk gt 65 years of age
  • But about 1/3 (28) are lt 65 years old
  • Tends to run in families
  • More often seen in females
  • More often seen in Blacks, perhaps due to
    increased incidence of hypertension

36
Three types
  • Global hypoperfusion shock
  • Ischemia thrombotic and embolic
  • Hemorrhagic

37
Risk Factors
  • Arterial hypertension
  • Heart disease
  • Myocardial infarction or endocarditis
  • Atrial fibrillation
  • Elevated plasma cholesterol
  • Diabetes mellitus
  • Oral contraceptives
  • Smoking
  • Polycythemia and thrombocythemia

38
Occlusive strokes
  • Occurs with blockage of blood vessel by a
    thrombus or embolus
  • May be temporary or permanent
  • Thrombotic stroke
  • 3 clinical types
  • TIAs
  • Stroke-in-evolution
  • Completed stroke

39
Transient Ischemic Attacks
  • Last for only a few minutes, always less than 24
    hours
  • All neurological deficits resolve
  • Symptom of developing thrombosis

40
Causes
  • Thrombus formation
  • Atherosclerosis
  • Arteritis
  • Hypertension
  • Vasospasm
  • Other
  • Hypotension
  • Anemia
  • Polycythemia

41
Symptoms depend on location
  • Ophthalmic branch of internal carotid artery
    amaurosis fugax fleeting blindness
  • Anterior or middle cerebral arteries
    contralateral monoparesis, hemiparesis,
    localized, tingling numbness in one arm, loss of
    right or left visual field or aphasia

42
Treatment
  • Without Tx 80 have a recurrence in symptoms, and
    1/3 go on to have a full stroke within 5 years
  • Give anticoagulants prophylactically , usually ½
    to 1 aspirin / day

43
Stroke-in-evolution
  • Can have abrupt onset, but develop in a
    step-by-step fashion over minutes to hours,
    occasionally, from days to weeks
  • Characteristic of thrombotic stroke or slow
    hemorrhage

44
Thrombotic CVA
  • Involves permanent damage to brain due to
    ischemia, hypoxia and necrosis of neurons
  • Most common form of CVA
  • Causes
  • Atherosclerosis assoc. with hypertension
  • Diabetes mellitus, and vascular disease
  • Trauma

45
  • May take years to develop, often asymptomatic
    until major narrowing of arterial lumen
  • Anything that lowers systemic B.P. will
    exacerbate symptoms (60 during sleep)
  • Area affected depends on artery and presence of
    anastomoses
  • Area affected initially is greater than damage
    due to edema
  • Infarcted tissue undergoes liquifaction necrosis

46
Embolic stroke
  • Second most common CVA
  • Fragments that break from a thrombus outside the
    brain, or occasionally air, fat, clumps of
    bacteria, or tumors

47
Common causes
  • Atrial fibrillation
  • Myocardial infarction
  • Endocarditis
  • Rheumatic heart disease and other defects

48
  • Impact is the same for thrombotic stroke
  • Rapid onset of symptoms
  • Often have a second stroke

49
Hemorrhagic Stroke
  • Third most common, but most lethal
  • Bleeding into cerebrum or subarachnoid space

50
Causes
  • Ruptured aneurysms
  • Vascular malformations
  • Hypertension
  • Bleeding into tumors
  • Bleeding disorders
  • Head trauma

51
  • Often a history of physical or emotional exertion
    immediately prior to event
  • Causes infarction by interrupting blood flow to
    region downstream from hemorrhage
  • Further damage by hematoma or IICP
  • Onset less rapid than embolic CVA, evolving over
    an hour or two

52
  • Usually chronic hypertension, and B.P. may
    continue to rise
  • About half report severe headache
  • In about 70 hematoma expands, destroying vital
    brain centers, shifts of brain tissue, and death

53
Degenerative Disorders
  • Progressive neurodisorders
  • Long-lasting
  • Permanent effects
  • Many present as syndromes
  • No cure, but much research

54
Alzheimer Disease (Dementia of Alzheimer Type)
55
Dementia is a loss of ordered neural function
  • Discrimination and attending to stimuli
  • Storing new memories and retrieving old
  • Planning and delay of gratification
  • Abstraction and problem solving
  • Judgement and reasoning
  • Orientation in time and space
  • Language processing
  • Appropriate use of objects
  • Planning and execution of voluntary movements

56
Course slow progression (5years or more)
  • At first affects only short term memory, but
    gradually extends to long term
  • Many experience restlessness
  • Many patients retain insight, which leads to
    anxiety and depression
  • Personality may be lost
  • Ultimately, mute and paralyzed
  • Death comes from infection

57
  • Onset may be as young as 50, and incidence
    increases with age
  • 6 of people over 65 years have AD
  • Almost half over 85 have AD
  • Diagnosis is by ruling out all other causes
    specific diagnosis only by biopsy or autopsy

58
  • Pathology restricted to cerebral cortex,
    hippocampus, amygdala, and another basal nucleus
    called nucleus of Meynert
  • Nucleus of Meynert produces Acetylcholine loss
    results in impaired neural function

59
Pathology
  • Pyramidal cells die loss of white matter
  • Gyri shrink and and ventricles and sulci expand
    walnut like appearance
  • Neurofibrillary tangles
  • Neuritic (senile) plaques filaments, microglia,
    astrocytes around core of amyloid
  • Amyloid angiopathy

60
http//www.ahaf.org/alzdis/about/plaques_tanglesBo
rder.jpg
61
www.infoaging.org/ d-alz-8-r-tangles.html
62
http//homepage.psy.utexas.edu/homepage/class/Psy3
32/Salinas/Disorders20/Disorders.html
63
  • About 10 of cases are familial, usually early
    onset
  • Gene on chromosome 21 carries gene for amyloid
    protein
  • Almost all people with Down syndrome who live
    beyond 45 years develop AD
  • Also linked to mutations on chromosomes 14 and 19
  • Prions have been isolated

64
Treatment
  • So far resistant
  • May revolve around amyloid protein
  • See high levels of aluminum chelating agents
    temporarily arrest or reverse some symptoms
  • THA(tetrahydroaminoacridine) used experimentally
    liver toxicity
  • Arthritics have lower incidence of AD
  • Therapy centers on problems of failing cognitive
    skills

65
Parkinson Disease movement disorder
  • Described over 180 years ago by James Parkinson
  • Combination of slowed, reduced movements and
    restless tremoring
  • Paralysis agitans
  • Slowly degenerative CNS disorder affecting 80,000
    adults in North America

66
Parkinson Disease
  • Degenerative disease of the basal ganglia
    involving the failure of dopamine-secreting
    neurons (substantia nigra)
  • Can be primary or secondary
  • Secondary caused by trauma, infection, neoplasm,
    atherosclerosis, toxins and drug intoxication

67
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68
Primary Parkinson Disease
  • Begins after the age of 40, with peak age of
    onset between 58 62
  • Course of 10- 20 years slowly progressive
  • More prevalent in males (slightly to 2X)

69
  • Substantia nigra two nuclei in midbrain
  • Outflow pathway from basal nuclei to cortex via
    thalamus
  • Damage impairs flow of motor programs
  • Expressed as difficulty initiating movements,
    general lack and slowing of movement
    (bradykinesia)

70
  • Loss of feedback loop impairs flow of programs
    and expresses as resting tremor
  • Most disabling symptoms are muscle rigidity and
    bradykinesia
  • Muscle strength is more or less normal
  • Poor balance
  • Face becomes immobile and inexpressive
  • Autonomic function is decreased
  • orthostatic hypotension, excess sweating,
    constipation, etc.

71
  • Some patients suffer dementia similar to
    Alzheimer Disease
  • Not fatal, but shortens life expectancy

72
Treatment
  • Active exercise and good nutrition
  • Strategies to overcome bradykinesia
  • Only when symptoms are severe are drugs given
    levodopa
  • Side effects cardiac arrhythmias,
    gastrointestinal hemorrhage, psychiatric
    problems, unpredictable involuntary movement
    disorders

73
Possible therapies
  • Foreign or autograft of tissue still
    experimental
  • Lesions in the subthalamic nucleus, thalamus or
    internal segment of globus pallidus promising
  • Stem cell research?

74
Multiple Sclerosis
  • Focal, chronic, progressive, usually exacerbating
    and remitting demyelination of CNS tracts.
  • Lesions can occur in a wide variety of locations
    and give rise to complex symptoms
  • Areas of demyelination are called plaques, and
    can occur anywhere oligodendrocytes provide
    myelin sheath

75
Onset
  • Onset is between 20 and 40 years, rarely before
    15 or after 50
  • Females Males 21

76
  • Clinical presentation depends on site of lesion
  • Involvement of optic nerve produces monocular
    visual disturbances first symptom in ¼ of
    patients
  • Half of people with optic neuritis are diagnosed
    with MS

77
Common symptoms
  • Double vision
  • Tingling in the back and anterior thigh upon neck
    flexion Lhermittes sign
  • Symptoms worsen when patient becomes heated
    Uhthoffs sign

78
Diagnosis
  • CSF obtained by lumbar puncture shows slight
    increase in protein on electrophoresis shows
    specific banding pattern antibodies within CSF
    suggest immune reaction
  • Changes in velocities of visual and auditory
    pathways
  • Plaques visible on MRI

79
Cause
  • Myelin undergoes breakdown and phagocytic
    destruction antibodies may play a role
  • Decreased signal conduction due to edema and
    demyelination that exposes potassium channels
    that short-circuit signal (edema resolves and
    have partial remyelination)

80
  • Epidemiology hints at interaction between a viral
    illness in the teen years and a genetic
    predisposition
  • Growing up in northern temperate climates
    increases rise
  • Non Asian heritage increases risk

81
Course
  • Pattern of exacerbation and remission
  • Stresses can trigger exacerbation infection,
    medication, stress, fatigue
  • Course is unstable and unpredictable
  • 10 undergo severe, rapid progressive
    deterioration
  • Some have died with 7 months of first symptom due
    to acute brain inflammation and infection

82
  • A significant number never severely incapacitated
  • Some experience only a single episode
  • Death is usually attributable to complications of
    MS (infections due to decreased function)

83
Symptoms
  • Increased urinary frequency
  • Lesions in frontal or temporal lobes can cause
    emotional outbursts
  • Depression and euphoria can be problems
  • Unpredictable progression taxes ability to cope
  • Occasionally, plaques can cause paraplegia or
    quadriplegia

84
Therapies
  • Only corticosteroids and ACTH appear to have
    effects reduce the duration of exacrerbation,
    but have no impact on long term outcome
  • Interferon ß
  • Maintaining a healthy lifestyle and outlook

85
Acute encephalopathies
  • Reyes Syndrome
  • First recognized in 1963
  • Characterized by encephalopathy and fatty changes
    in several organs, esp. liver
  • Incidence has declined in past 20 years due to
    awareness of ingestion of aspirin during illness
    and development of Reyes syndrome.

86
Reyes syndrome
  • Typically develops in a healthy child of 6 mo. to
    15 years recovering from varicella, influenza B,
    upper respiratory tract infection, or
    gastroenteritis.
  • Stage I vomiting, lethargy, drowsiness
  • Stage II disorientation, delirium,
    aggressiveness and combativeness, central
    neurological hyperventilation, shallow breathing,
    hyperactive reflexes, stupor

87
Reyes syndrome
  • Stage III Insensitivity to pain, coma,
    hyperventilation, rigidity
  • Stage IV deepening coma, loss of ocular
    reflexes large, fixed pupils divergent eye
    movements
  • Stage V seizures, loss of deep tendon reflex,
    flaccidity, respiratory arrest
  • Mortality is 10 or more
  • Formerly 40 to as high as 80
  • In a few cases death is due to liver failure

88
Reyes syndrome
  • Cause
  • May have a genetic predisposition
  • May be due in part to exhaustion of glycogen
    stores and use of fatty acids -Mitochondrial
    injury
  • Treatment
  • Aggressive intensive care
  • Treatment for brain edema and IICP
  • Fluids I.V. and control of blood electrolytes
  • Prevent hyperthermia

89
Seizure disorders
  • Seizure is and abnormal discharge of electrical
    activity within the brain. It is a rapidly
    evolving disturbance of brain function that may
    produce impaired consciousness, abnormalities of
    sensation or mental function or convulsive
    movements.
  • Convulsions are episodes of widespread and
    intense motor activity

90
Epilepsy
  • A recurrent disorder of cerebral function marked
    by sudden, brief attacks of altered
    consciousness, motor activity or sensory
    phenomenon.
  • Convulsive seizures are the most common form
  • Some, but not all, recurrent seizures are due to
    epilepsy

91
Epilepsy
  • Second most common neurological disorder
  • Incidence increases with age, with 30 initially
    occurring before 4 years and 75 -80 before 20
    years.
  • Causes brain tumor, scar tissue, neurological
    disease, great majority of cases are idiopathic.

92
  • Signs and symptoms vary
  • petit mal almost imperceptible alterations in
    consciousness
  • grand mal generalized tonic-clonic seizures
    dramatic loss of consciousness, falling,
    generalized tonic-clonic convulsions of all
    extremities, incontinence, and amnesia for the
    event.

93
  • Some attacks are proceeded by a prodrome a set
    of symptoms that warn of a seizure
  • As the seizure begins, the patient may experience
    an aura mental, sensory or motor phenomena
  • Others have no warning

94
Phases of a grand mal seizure
  • Tonic phase ( 10 -20 seconds) muscle
    contraction
  • Epileptic cry respiration stops
  • Clonic phase (1/2 -2 minutes) muscle spasms
    respiration is ineffective autonomic nervous
    system active
  • Terminal phase (about 5 minutes) limp and quiet,
    EEG flat lines

95
  • 5-8 are at risk of status epilepticus a
    series of GTCS without regaining consciousness
    medical emergency
  • Seizure activity lasts more than 30 minutes
  • Acidosis
  • Elevated pCO2
  • Hypoglycemia
  • Fall in blood pressure
  • Can lead to severe brain damage or death

96
Epileptogenic focus
  • Group of brain neurons susceptible to activation
  • Plasma membranes may be more permeable to ion
    movement
  • Firing of these neurons may be greater in
    frequency and amplitude
  • Electrical activity can spread to other
    hemisphere and then to the spinal cord

97
Treatment
  • Treat any underlying metabolic disorders, or
    tumors
  • Most cases can be controlled through routine use
    of antiepileptic medications usually only one
    drug to minimize side effects
  • Surgical intervention if drugs ineffective
  • Supportive therapy patients learn to cope
    effectively with stress, eat well, and get
    sufficient rest and avoid triggers.

98
Eliciting stimuli
  • Hypoglycemia
  • Fatigue
  • Emotional or physical stress
  • Fever
  • Hyperventilation
  • Environmental stimuli

99
  • Patients are normal between attacks
  • Can participate in sports, drive a car (if no
    seizures for 6 mo 1 year)
  • Should not drink alcohol
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