MID 2: NEURO Flashcards
Cranium
protects brain and associated structures
Meninges
3 protective membranes – the dura mater, the arachnoid, and the pia matter - subdural space lies between the dura and arachnoid – subarachnoid space lies between the arachnoid and pia layers – this contains the cerebrospinal fluid
Cerebrospinal fluid
intracranial and spinal structures float in the CSF – protected from injury – 125 – 150 ml CSF is circulating in the subarachnoid space and ventricles – 600 mls produced daily – CSF is formed in the ventricles circulated through the ventricles and then reabsorbed into the venous system through the arachnoid villi
Pupillary changes
indicate brainstem dysfunction – brainstem control of arousal is adjacent to areas that control pupils – However, you need to consider that some medications will also affect the pupils
Oculomotor responses
Abnormal eye movements, including nystagmus indicate alterations in brainstem function.
eyes should move together – dysconjugate movement - or no eye movement is indication of brain injury
Motor responses
can be classified as purposeful, inappropriate, or not present – patients are asked to “squeeze my fingers” to determine their motor response – inappropriate responses include decerebrate and decorticate posturing
decorticate – flexion –( bringing into the core )– is associated with hemispheric damage above midbrain
decerebrate – extending away – is associated with severe damage involving the midbrain and upper pons
Patterns of breathing
normally our forebrain produces a rhythmic pattern of breathing – if the LOC decreases the brain relies on CO2 levels to regulate respiration – CO2 climbs so respiration is increased – increased respiration decreases CO2 levels so respiration rate decreases – Cheyne stokes pattern
Glasgow Coma Scale (GCS)
- eye-opening response
- verbal response
- motor response
Selective attention
- ability to focus – we can choose what we are going to pay attention to
- selective attention deficits can be caused by seizures, contusions, subdural hematomas, stroke neoplasms, Alzheimer’s disease, dementia
- Temporary, permanent, or progressive
Amnesia
mild or severe loss of memory
Retrograde amnesia
difficulty with past personal history or facts
Anterograde amnesia
inability to form new memories
Agnosia
defects of recognition and may be tactile, visual, or auditory. They are caused by dysfunction in the primary sensory area or the interpretive areas of the cerebral cortex. Usually only one sense is affected.
Dysphasia (aphasia)
an impairment of comprehension or production of language
Broca’s area
cannot create speech
Wernicke’s area
cannot comprehend speech
Intracranial hypertension 4 stages
In stage 1 the brain is trying to compensate - mainly through vasoconstriction - in this stage the patient may be asymptomatic
In stage 2 the intracranial pressure is increasing beyond the ability of the brain to compensate - cellular hypoxia worsens - the body attempts to compensate through systemic vasoconstriction - the patient will start to show signs of increased ICP - confusion and restlessness, decreased level of consciousness
In stage 3 the intracranial pressure is approaching arterial pressure - cellular hypoxia worsens, patient becomes hypercapnic. The patient will decompensate quickly at this point, intervention is required quickly. Patient will show decreased level of consciousness, widening pulse pressure, decreased heart rate, pupils will be small and sluggish
In stage 4 the brain is herniating. ICP equals arterial pressure which prevents cerebral perfusion, hypoxia leads to cellular death which will further increase ICP - patient is past the point of recovery. pupils will be unequal and will eventually be fully dilated “blown pupils” BP, HR, will decreased, Cheyne-stoke breathing
Cushing’s triad
- increased BP, decreased pulse rate, irregular breathing rate
- occurs in late stages of acute head injury
- indicates that brain stem herniation is imminent
Hypotonia
decreased muscle tone – passive movement of a muscle has little resistance if any
Hypertonia
increased muscle tone – passive muscle movement with resistance to stretch
Hyperkinesia
excessive purposeless movements - could be tremors, or abnormal involuntary movements
Dyskinesia
abnormal movements that occur as spasms – tardive dyskinesia is movements of the face – Tourette’s syndrome – unwanted tics
Hypokinesia
loss of voluntary movement – decrease or slowness of voluntary movements – delay in time that it takes to start to perform a movement
Spinal shock
- is the temporary loss of all spinal cord function below the level of the lesion – consequence of spinal cord injury – initial reaction is
- Complete paralysis, absence of reflexes, motor, sensory, autonomic function, including disturbances in bowel and bladder function – can last hours to weeks
- over time spinal shock will resolve – damage to spinal cord remains – so initially they may have loss of all function, but as their reflexes return we get a clearer picture of what damage has been done
- Return of spinal reflexes marks the end of spinal shock
Paresis
condition of muscle weakness caused by nerve damage or disease – partial paralysis – can be confined to one area – limb or lower body or can be general or progressive as we may see in dementia
Paralysis
loss of muscle function in part of your body
Hemiparesis/hemiplegia
- one-sided muscle weakness
- upper and lower on one side
- stroke
Diplegia
paralysis of corresponding parts of both sides of the body – cerebral hemisphere injuries of specific part of the brain
Paraplegia
weakness or paralysis of lower extremities due to spinal cord injury
Quadriplegia
weakness or paralysis of all four extremities due to spinal cord injury – looking at this in our spinal cord trauma
Brain death
- brain is damaged beyond the point of recovery– brainstem functions have stopped – etiology is not reversible
- absence of motor responses, no spontaneous respirations, no brain functions – doll’s eyes(comatose patient’s brainstem is not intact)., corneal reflex, ice in ears
Cerebral death
or irreversible coma, represents permanent brain damage, with an ability to maintain cardiac, respiratory, and other vital functions - person does not speak, open their eyes or have purposeful movements
Vegetative state
Arousal returns in vegetative states, but awareness is absent.– does not speak or understand speech, cannot follow commands, but sleep-wake cycles present, has spontaneous eye opening– vegetative states that last longer than 12 months are considered permanent
