Increased Intracranial Pressure

(IICP)

may result from anything that takes up volume in the brain

eg. tumuor, edema, excess CSF or hemorrhage

Stage 1: Vasoconstriction and external compression of the venous system occur in order to decrease the ICP (may be asymptomatic)

Stage 2: when continuing swelling exceeds this compensatory mechanism, oxygenation is compromised (confusion, drowsiness), and systemic vasoconstriction occurs to increase systemic blood presure in order to overcome decreased flow in the brain

Stage 3: with continued swelling, when ICP begins to equal arterial pressure, cerebral perfusion pressure falls, and hypoxia and hypercapnia of brain tissue occur (rapid deterioration: small sluggish pupils); all compensatory mechanisms have been used and dramatic rise in ICP over a very short period of time

Stage 4: brain tissue shifts (herniates) from the compartment of greater pressure to a compartment of lesser pressure; this increases pressure in the lower compartment and impairing its blood supply; therefore, ICP increased to where it equals systolic arterial pressure at w/c point cerebral blood flow ceases

- an increase in the fluid content of brain tissue

- occurs after trauma, infection, hemorrhage, tumour

- distorts blood v., displaces brain tis, causes herniation

- caused by:

- increased permblty of BBB

- toxins cause failure of transport mechanism of cells so more Na+ inside cell and more H20 inside cell: occurs in gray matter

- obstruction of circulation of CSF in ventricles so fluid leaks into surrounding brain tissue

- excess fluid in ventricles, subarachnoid space, or both

- caused by:

- too high production of CSF eg. tumour in choroid plexus

- obstructed flow thru ventricles eg. aqueduct stenosis

- too low reabsorption of CSF eg. interference w/ arachnoid villi

- develops over time but can occur rapidly as a result of brain injury

1. alterations in muscle tone

- can result in a spectrum fr. flaccidity (hypotonia) to rigidity (hypertonia)

- dystonia - sustained invol. twisting movement of the hand and foot

2. alterations in movement

- paresis

- paralysis

- hyperkinesia

3. alterations in complex motor performance

- includes 3 types:

- disorders of posture: decorticate, decerebrate

- disorders of gait: spastic gait

- disorders of expression: hypermimesis, dyspraxia/apraxia

- loss of motor neuron fxn so that a muscle gr. is unable to overcome gravity

- occur in both upper (brain/spinal cord) and lower (cranial/spinal nerves) motor neurons

- for upper: hemiparesis/hemiplagia, paraparesis/paraplagia, quadriparesis/quadriplegia

- excessive movements eg. tremors, tics

- due to physical or chemical causes eg. insufficient dopamine

- upper extremities flexed at the elbows and held close to the body and lower extremities are externally rotated and extended

- may occur w/ cerebral hemisphere damage

- increased tone in extensor muscles and trunk muscles, w/ clenched jaw and extended neck so head in neutral position, all four limbs rigidly extended

- occurs w/ brain stem lesions

- a shuffling gait w/ leg extended and held stiff

- inability performing tasks that require learned motor skills (speaking, writing, using tools, following instructions)

- problem is w/ use of muscles, not w/ comprehension

- dura remains intact

- may result in both focal brain injuries (one area) or diffuse axonal injuries (more than one area)

- break in the dura

- resulting in exposure of the cranial contents to the environment

- bruises in brain tissue

- blood leaking fr. injured blood vessels

- edema occurs around/in damaged area as well as infarction, necrosis, hemorrhage

- effects peak 18-36 hr after injury

- sequence of events:

- immediate loss of consciousness

- loss of reflexes

- brief period of no respiration

- brachycardia

- decrease in BP

- vital signs may stabilize in a few sec.

- reflexes and consciousness return

- residual effects may persis

- eg. extradural (epidural) hematomas, subdural hematomas, intracerebral hematomas

- impact against the object, causing direct trauma to brain at point of impact

- impact w/in skull, causing impact injury at area opposite to object, and shearing forces through the brain

- fr. head bouncing off object of initial impact

- injury causes bleeding bet. the dura mater and the skull due to arterial bleeding

- bleeding bet. the dura mater and the brain

- acute caused by traumatic injury develop rapidly, commonly w/in hrs

- chronic (due to accompanying cond.) develop over weeks to months

- bleeding w/in the brain

- penetrating injury or shearing forces traumatize small blood v.

- may be delayed, appearing 3-10 days after injury

- projectiles and debris fr. scalp and skull injury/fracture penetrate dura mater

3 Mechanisms produce brain damage

1. Primary

a. focal brain injury: contusions - coup, contrecoup

- ex of contusions:

- extradural hematomas

- subdural hematomas

- intracerebral hematomas

- penetrating brain trauma

b. diffuse brain injury: diffuse axonal injury (DAI) - concussion

- categories:

- mild concussion

- classic cerebral concussion

- mild DAI

- moderate DAI

- severe DAI

2. Secondary - indirect result of primary trauma

- mechanisms:

- cerebral edema

- IICP

- decreased cerebral perfusion pressure

- ischemia

- brain herniation

- brain damage occurs hrs. to days after primary trauma

3. Tertiary

- specific, grossly observable brain lesions that occur in a precise location

- concussion, result of shaking, rotational and twisting movements

- involves widespread area of the brain, w/ damage to axonal fibers - can be observed only with microscope

- reduces the speed of informational processing

- no loss of consciousness but CSF pressure increases

- confusion lasts for several mins, retrograde amnesia

- loss of consciousness for up to 6 hr. 

- confused state lasts for several hrs., headache, nausea, retrograde amnesia

- 6-24 hr coma

- may display decerebrate or decorticate w/ extended periods of stupor/restlessness

- >24hr coma

- may display above posturing w/ unconsciousness lasting days or weeks

- on awakening, permanent deficit in memory, reasoning, language, etc.

- emerge fr. coma in the first 3 months after injury

- initial injury eventually results in compromised coordinated movements, verbal and written communication skills, inability to learn and reason

- abnormality of the brain caused by a pathologic process in the blood v. 

- vessel wall lesions

- occlusion of the v. lumen by thrombus or embolus

- rupture of the v.

- alteration in blood quality eg. increased blood viscosity

- result can be either ischemia w/w/o infrctn/hmorrhage

- leads to cerebrovascular accident or stroke

- risk factors: arterial hypertension, smoking, diabetes, insulin resistance, polycythemia

- occlusions formed by thrombi developing in arteries supplying the brain

- develop as a result of atherosclerosis, after plaque ruptures and a clot is formed

- piece of thrombus detaches and lodges in vessel upstream, causing acute ischemia

Transient ischemic attack

(TIA)

- a brief episode of neurologic dysfunction caused by a focal disturbance of brain w/ symptoms lasting less than 1 hr, no evidence of infarction and complete clinical recovery

- result of platelet clumps or vessel narrowing w/ spasm, causing an intermittent blockage of circulation

- no treatment, high risk of repeat occurrence and eventual stroke

- involves fragments that break fr. a thrombus formed outside the brain

- may plug lumen of small vessel entirely or may shatter

- a second stroke usually follows b/c the source of emboli continues to exist

- a mass of blood forms and grows to displace adjacent brain tissue

- associated w/ increased systolic and diastolic pressures over several years

- causes include hypertension, ruptured aneurysms, trauma

- size vary fr. 2mm-2/3cm, classified on the basis of shape

- asymptomatic; first indication is an acute subarachnoid hemorrhage and/or intracerebral hemorrhage

- rupture thru thin areas, causing hemorrhage, producing local changes in cerebral cortex

- produces painful headache or unconsciousness or both

- acquired autoimmune inflammatory disorder

- involves destruction of axonal myelin in the CNS

- onset usually bet. 20-40 yrs/more common in women

- symptoms include paresthesias of the face, trunk or limbs, weakness, visual disturbances

Alzheimer Disease

- most common causes of severe cognitive dysfunction in older persons and the leading cause of dementia

- cause is unknown

- plaques form bet. neurons and protein containing tangles form inside neurons, damaging and killing neurons, disrupting nerve impulse transmission

- forgetfulness, emotional upset/illness, memory loss, behavioral changes

- no cure

1. Thrombotic stroke - occlusions by thrombi in arteries supplying the brain

2. Embolic stroke - fragments that break fr. a thrombus formed outside the brain

3. Hemorrhagic stroke - mass of blood forms and grows to displace adjacent brain tissue

1. Structure: infections, neoplasms, trauma, etc.

2. Metabolism: hypoxia, drugs, electrolytes disturbances

3. Psychogenic: uncommon, through psychiatric disorder

- a method used for assessing level of consciousness in person w/ brain injury

- numbered scores given to responses of eye opening, verbal utterances, and motor responses

Evaluation of arousal

- to determine the extent of brain dysfunction

1. level of consciousness

2. patterns of breathing

3. pupillary changes

4. oculomotor responses

5. motor responses

Persistent vegetative state

(PVS)

- complete unawareness of self or the surrounding environment

- sleep-wake cycles are present, brain stem reflexes are intact but bowel and bladder incontinence

- complete paralysis of vol. muscles except the eye movements

- fully consciousness w/ intact cognitive fxn but can't communicate thru speech or body movements

1. brain death - no recovery

2. cerebral death - irreversible coma

3. PVS - unawareness of self and environment

4. minimally conscious state - follow simple commands

5. locked-in syndrome - paralysis of vol. muscles

- include all cognitive fxns

- caused by destruction of tissue caused by hypoxia/ischemia or compression, or effects of toxins/chemicals

- involved:

- selective attention

- memory

- executive attention deficits

- sudden temporary change in motor, sensory, autonomic or psychic clinical manifestations and a temporary altered level of arousal - convulsions (jerky movements)

- results fr. a sudden, explosive, disorderly discharge of cerebral neurons

- caused by cerebral lesions, biochemical disorder, cerebral trauma and epilepsy

- inability to recognize the form/nature of objects

- affects one sense

- caused by any damage to a specific part of the brain

- inability to understand or use of symbols (written/verbal)

- caused by dysfuxn in left cerebral hemisphere

- inability to concentrate on incoming sensory info.; highly distractible

- caused by drug intoxication, nervous system disease, trauma, surgery, etc.

- progressive failure of cerebral functions such as orienting, memory, language, judgment and decision-making

- accompanied by behavioral alterations

- caused by neuron degeneration, atherosclerosis, trauma, infection

1. inadequate cerebral perfusion

2. normal cerebral perfusion w/an elevated intracranial pressure

3. excessive cerebral blood volume