15. Neuro: Cognitive Systems & Cerebral Hemodynamics Flashcards
absence of voluntary movement
akinesia
damage between fibers of language center – may not be able to control tone and emotions of language
transcortical dysphasia
muscle resistance to passive movement of a rigid limb that is uniform in both flexion and extension throughout movement
rigidity
ICP may not change in this stage due to compensatory mechanisms
Stage 1 IICP
Cause of hydrocephalus
interference of CSF flow - decreased reabsorption - increased production - obstruction within ventricular system
AD hereditary degenerative disorder that causes severe degeneration of basal ganglia and frontal cerebral atrophy -> depletion of basal ganglia GABA (inhibitory NT)
Huntington disease (HD or Chorea)
inability to remember instructions and information needed to guide behavior
working memory deficit
broad-based gait where person walks in small steps and the head and body are flexed -> due to basal ganglion dysfunction and seen in Parkinson disease
basal ganglion gait
weakness/paralysis of lower extremities as a result of lower spinal cord injury
paraparesis/paraplegia
Broca vs Wernicke
- Broca’s area: helps in producing coherent speech - Wernicke’s area: helps in speech processing and understanding language
Explain the rhythm of Cheyne-Stokes respiration
- increased levels of CO2 -> tachypnea - CO2 levels decrease -> leads to apnea until CO2 accumulates again
agnosia is commonly associated w/ what neurological problem
CVA
Clinical manifestations of stage 3 IICP
- decreased levels of arousal - widened pulse pressure (systolic increases) - bradycardia - small, sluggish pupils
4 criteria for brain death
- unresponsive coma (no motor or reflex movements) - no spontaneous respiration (apnea) - no brainstem functions (dilated, fixed pupils; no gag or corneal reflexes) - isoelectric EEG
loss of emotional language (aprosody); inability to understand emotional in speech and facial expression or inability to express emotion
hypomimesis
result due to damage of descending motor pathways
upper motor neuron syndromes
associated w/ upper motor neuron syndromes; mainly the flexors of the arms and extensors of the legs are affected
pyramidal motor syndrome
involves an inability to understand written or spoken language; speech is fluent but words and phrases have no meaning
Receptive dysphasia or Wernicke’s/sensory/fluent dysphasia
defect of pattern recognition -> failure to recognize the form and nature of objects (can be tactile, visual, or auditory)
Agnosia
more severe form of dysphasia and an inability to communicate using language; usually associated w/ CVA involving the middle cerebral A.
aphasia
Indicates the presence and level of brainstem dysfunction
pupillary changes
causes of increased intracranial pressure (IICP)
increased intracranial content - tumor growth - edema - excessive CSF - hemorrhage
excessive, purposeless movement (broad category of abnormal movements)
hyperkinesia
neurodegenerative disorder that diffusely affects upper and lower motor neurons of the cerebral cortex, brain stem, and spinal cord (corticospinal tracts and anterior roots)
amyotrophic lateral sclerosis (ALS or Lou Gehrig disease)
acquired mental disorder characterized by deficits in attention and coherence of thought and action; secondary to intoxication, metabolic disorders, or nervous system disorders
acute confusional states (ACS); may also be called delirium
complete unawareness of the self or surrounding environment and complete loss of cognitive function; can be seen in survivors of cerebral death
persistent vegetative state (VS)
complete paralysis of voluntary muscles except for eye movements; person cannot communicate through speech or body movement but is fully conscious w/ intact cognitive function
locked-in syndrome
isolated contraction of a single muscle fiber because of metabolic changes I denervated muscle -> not clinically visible
fibrillation
individuals may follow simple commands, manipulate objects, gesture or give yes/no responses, have intelligible speech, and have movements such as blinking/smiling
minimally conscious state (MCS)
loss of motor function so that a muscle group is unable to overcome gravity
paralysis
muscle rippling or quivering under the skin
fasciculations
sustained involuntary muscle contraction that causes twisting movement
dystonia
Clinical manifestation of ALS
progressive muscle weakness leading to respiratory failure and death; pt has normal intellectual and sensory function until death
resistance to passive movement which varies in direct proportion to force applied
paratonia
Classic manifestations of PD
- resting tremor - rigidity - bradykinesia/akinesia - postural disturbance (stooped) - short shuffling steps - cognitive-affective symptoms
occurs when the brain is damaged so much that it can never recover (irreversible) and cannot maintain internal homeostasis
Brain death
large motor neurons in ventral horn of spinal cord -> bring nerve impulses from upper motor neurons to the skeletal muscle through anterior spinal roots and cranial nerves
lower motor neurons
NT necessary to make muscle tone smooth
dopamine
normal ICP
5-15 mmHg
posture/response caused by severe injury to the brain/brainstem
decerebrate posture/response
sleep-wake cycle are present, eyes open spontaneously, and BP and breathing are maintained without support; brainstem reflexes intact but cerebral function lost
persistent vegetative state (VS)
stage of IICP where brain tissue herniates from compartment of greater pressure to compartment w/ less pressure -> blood supply compromised -> further hypoxia in herniated tissues
Stage 4 IICP
paralysis of corresponding parts of both sides of the body as a result of cerebral hemisphere injuries
diplegia
cerebral edema caused by increased permeability of capillary endothelium of brain after injury to vascular structure (BBB is disrupted)
vasogenic edema
paresis/paralysis of the upper and lower extremities on one side
hemiparesis/hemiplegia
inability to form new personal or factual memories but memories of distant past are retained
anterograde amnesia
executive attention deficits are associated w/ alternations to which area of the brain?
frontal and prefrontal cortex
death of the cerebral hemispheres exclusive of the brain stem and cerebellum (no behavior or environmental responses but brain can maintain homeostasis)
Cerebral death (irreversible coma)
excess fluid within the cranial vault, subarachnoid space, or both -> causes dilation of ventricles and IICP -> severe headache
hydrocephalus
posture/response characterized by increased tone in extensor muscles and trunk muscles w/ active tonic neck reflexes (head is neutral and all 4 extremities are rigidly extended)
decerebrate posture/response
inability to set goals and recognize when an object meets a goal
sustained attention deficit
progressive deterioration of cerebral functions due to neurofibrillary tangles and plaques -> lead to neuronal death and brain atrophy
Alzheimer’s disease (AD)
decreased amplitude of movement
hypokinesia
stage with continued expansion of intracranial contents and pressure may compromise neuronal oxygenation and systemic arterial vasoconstriction may occur to overcome IICP
Stage 2 IICP
At what stage of IICP is surgical or medical intervention the best?
Stage 2 IICP
loss of ability to perform activities that a person is physically able and willing to do -> brain is unable to make and deliver correct movement instructions to the body
dyspraxia/apraxia
follows an epileptic seizure and can last hours or 1-2 days; includes headache, confusion, dysphasia, memory loss, and fatigue/deep sleep
postictal state
state of continuous seizures lasting more than 5 minutes or rapidly recurring seizure before the person has regained consciousness
status epilepticus
Diagnostic hallmark of PD? What does it lead to later in disease?
- Lewy body formation in neurons (protein misfolding and accumulation of alpha-synuclein) - Lewy body dementia later in disease
gait associated w/ bilateral upper motor neuron injury and spasticity -> when walking, legs swing around the body and then cross in front of each other
scissors gait
posture/response that occurs when the brainstem is not inhibited by the cerebral cortex motor area
decorticate posture/response
Clinical manifestations of stage 4 IICP
- progression to deep coma - ipsilateral dilation and fixation of pupils -> bilateral dilation and fixation of pupils - abnormal breathing (Cheyne-stokes, ataxic, or central neurogenic hyperventilation) - pulse pressure begins to decrease (as brain herniates and ICP decreases) - pulse slightly irregular
Motor signs that indicate loss of cortical inhibition
primitive reflexes and rigidity (paratonia)
5 patterns of neurologic function that are critical to evaluate
- level of consciousness - pattern of breathing - pupillary reaction - oculomotor responses - motor responses
exaggerated emotional response; excessive crying (left hemisphere) or laughing (right hemisphere); may not be appropriate to environment
hypermimesis
2 symptoms of the preictal phase of a generalized tonic-clonic seizure
- prodroma: hours to days before (anxiety/depression, inability to think clearly) - partial seizure: immediately precedes generalized seizure
difficulty retrieving past personal history memories or past factual memories
retrograde amnesia
gradual increase in tone causing increased resistance until tone suddenly diminishes
spasticity
severe degeneration of basal ganglia involving dopaminergic nigrostriatal pathway -> dopamine deficiency (inhibitory NT) and unopposed cholinergic activity (promotes muscle tone)
Parkinson disease (PD)
posture/response characterized by upper extremities flexed (held close to body) and lower extremities that are externally rotated and extended
decorticate posture/response
stage where ICP begins to reach arterial pressure and brain tissues experience hypoxia and hypercapnia -> rapid deterioration
Stage 3 IICP
increased fluid (intracellular or extracellular) within the brain
cerebral edema
decreased speed of movement
bradykinesia
abnormal, involuntary movements that occur in spasms
paroxysmal dyskenisias
Clinical manifestations of stage 2 IICP
subtle and transient - confusion - restlessness - drowsiness - slight pupillary and breathing changes
involves loss of ability to produce spoken or written language w/ slow or difficult speech
Expressive dysphasia or Broca’s/motor/nonfluent dysphasia
wide-based gait w/ increased body sway and falls, loss of truncation motion, and shuffling
frontal lobe ataxic gait
passive movement of a muscle mass w/ little to no resistance
hypotonia
temporary loss of all spinal cord functions below the lesion
spinal shock
gait associated w/ unilateral upper motor neuron injury -> manifests by a shuffling gait w/ leg extended and held stiff (scrapes floor surface)
spastic gait
impairment of comprehension or production of language w/ impaired communication
dysphasia
Clinical manifestations of lower motor neuron syndromes
- flaccid paralysis (both involuntary and voluntary movements affected) - hyporeflexia or areflexia (loss of tendon reflexes) - fibrillation
partial paralysis w/ incomplete loss of muscle power
paresis
clinical manifestations of AD
- forgetfulness - emotional upset - confusion - lack of concentration - decline in abstraction, problem solving, and judgement
explain the phases of a tonic-clonic seizure
- neurons are hypersensitive (fire more frequently and w/ greater amplitude - when intensity reaches a threshold point -> cortical excitation spreads - tonic phase (muscle contraction w/ increased muscle tone) - clonic phase (alternating contraction and relaxation of muscles) -> begins when inhibitory neurons in cortex react to excitation
gait that is wide-based w/ feet apart and often turned inward for greater stability (person staggers) -> due to cerebellar dysfunction
cerebellar (ataxic) gait
inability to maintain sustained attention and a working memory deficit
executive attention deficits
involuntary movement of the face, lips, tongue, trunk, and extremities
tardive dyskinesias
increased muscle resistance to passive movement
hypertonia
paresis/paralysis of all 4 extremities as a result of upper spinal cord injury
quadriparesis/quadriplegia
