PATHOPHYSIOLOGY OF MENINGITIS

INFECTION/INFLAMMATION OF THE

MENINGES COVERING THE BRAIN AND SPINAL CORD.

Infective organisms enter the CNS

Organisms quickly disseminate into the meninges and ventricles

Dissemination result in:

 Meningeal congestion, cerebral edema, increases ICP, pus formation. 

 Ø INFANT: hydrocephalus happens, if exudates block ventricles. 

Skull is capable of expanding.

Ø ADULT: blockage of the ventricles would to increases ICP.

PATHOPHYSIOLOGY OF HUNTINGTON'S DISEASE

hereditary disease that causes degeneration of cerebral cortex and basal ganglia.

Involves disturbance in neurotransmitter substance primarily 

> Gamma Aminobyutric Acid (GABA)

> Dopamine 

GABA neurons in basal ganglia, frontal cortex and cerebellum are destroyed

 GABA neurotransmitter production 

Excess of dopamine causes abnormal nerotransmisson along

the affected pathway

Chorea and mental deterioration

Enlargement of the ventricles in HD patients due to atrophy of 

the head of the caudate from neuronal loss.

PATHOPHYSIOLOGY OF BELL'S PALSY

Disorder CN VII unilateral facial paresis/paralysis

Compression of the facial nerve 

due to demyelination.

Inflammation or ischemia (inadequate blood supply)

The facial nerve is responsible for contraction

of the muscle of the face in expression, lacrimation

and the senses of taste and hearing.

PATHOPHYSIOLOGY OF ALZHEIMER'S DISEASE

 progressive degeneration and atrophy of brain. 

The brain of patients with alzheimer’s has 3 distinguishing features

Neurofibrillatory tangles (fibrous protein)

Amyloid plaques (composed of degenerating axons and dendrites)

Granulovacuolar degeneration(fibrous protein)

Normal brain weighs 1,380 g

>autopsy of alzheimers brain
>reveals brain atrophy
>weighs 1,000 g or less (fibrous protein)

PATHOPHYSIOLOGY OF INCREASED INTRACRANIAL PRESSURE

 increase in any three intracranial components.






EDEMA

INCREASED INTRACRANIAL PRESSURE

BLOOD VESSEL COMPRESSION

DECREASED PERFUSION

DECREASED OXYGEN

BRAIN CELL DEATH

PATHOPHYSIOLOGY OF GUILLAINE BARRE SYNDROME

An acute, rapidly progressive and fatal form of polyneuritis. 

WHITE BLOOD CELLS (WBC) ATTACK PERIPHERAL NERVES

DESTRUCTION OF MYELIN SHEATH (DEMYELINATION)

WIDENING OF THE NODES OF RANVIER

DELAY OR IMPAIRMENT OF IMPULSES TRANSMISSION

WEAKNESS / PARALYSIS / LOSS OF SENSATION

PATHOPHYSIOLOGY OF MULTIPLE SCLEROS

A progressive demyelination of the white mater of the brain and spinal cord.

INFECTION / AUTOIMMUNE RESPONSE

ATTACKS WHITE MATER OF BRAIN

DESTRUCTION OF MYELIN SHEATH

SCARRING (GLIOSIS, HARD YELLOW PLAQUES)

DISRUPTION OF NERVE CONDUCTION

NEUROLOGIC DYSFUNCTION