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neurologic and psychiatric disorders
Terms in this set (95)
transient loss of consciousness due to reduced cerebral blood flow
In general why does syncope occur?
my be benign as a result of a normal cardiovascular reflex or malignant when due to life-threatening arrhythmia. Results from a sudden impairment of brain metabolism usually brought about by hypotension and a reduction in cerebral blood flow
What are the 3 general mechanisms for the decreased cerebral blood flow in syncope?
1) disorder of vascular tone or blood volume-classic "faint" due to standing, etc. 2) cardiovascular disorder-particularly cardiac arrhythmias 3)cerebrovascular disease-rarely alone causes syncope
numerous subjective descriptors including lightheadedness, faintness, spinning, giddiness.
What are the 3 categories of dizziness?
1) faintness- presyncope; prodromal symptoms reflecting ischemia but not enough to cause loss of counsciousness 2) Vertigo- disturbance in the vestibular system 3) miscellaneous head sensations
neural output is conveyed in the vestibular nuclei in the brainstem; disturbance in the vestibular system; inner ear components transduce information on movement, graviational forces and head positioning in space
Vestibular Reflex (VOR)
serves to maintain visual stability during head movement
this occurs when the sensory systems encounter a novel situation such as sea and space sickness or unusual head/neck positioning such as in painting a ceiling
dysfunction of the vestibular system; accompanied by nausea, jerk nystagmus, unsteadiness and gait ataxia
Positive abnormal sensory phenomena
representing enhances or excessive activity in sensory pathways- tingling (among many other descriptors)
Negative abnormal sensory phenomena
representing loss of sensory function-numbness
tingling, pins-and-needles, etc.
more general term to cover all types of abnormal sensations
reduction in cutaneous sensation
complete absence of skin sensation
reduced pain perception
pain in response to touch
severe pain in response to mildly noxious stimulus
simulates light sleep, characterized by easy arousal and persistence of alertness for brief periods; usually some confusion present
degree of unarousability requiring vigorous stimuli to be awakened; confusion present
deep sleep-like state from which a person cannot be aroused
awake but unresponsive; typically has emerged from a coma; cardiac arrest and head injuries most common cause
what are the 5 categories of clinical evaluation for neurologic function?
1) level of consciousness 2) pattern of breathing 3) size and reactivity of pupils 4) eye position and reflexive responses 5) skeletal muscle motor responses
what brain system mediates changed in emotions and mood?
mediated primarily by the limbic system
what is the general cause for change in the limbic system?
primary causes include: abscesses, tumors, hemmorrhage, metabolic disorders, degenerative disease, intoxication
What is the critical variable to maintain for normal brain function? Through what 3 blood dynamics is it regulated?
The critical variable to maintain normal blood function is OXYGENATION. it is regulated by 1) cerebral blood volume 2) cerebral blood flow 3) cerebral perfusion pressure
What are the 3 typical changes seen in brain injury?
1) cerebreal oligemia 2) normal CPP with elevated intracranial pressure (ICP; normal is 5-15mmHg) tumors, edema, excess CSF, hemorrhage 3) cerebral hyperemia
Describe the 4 stages of increased ICP and intracranial hypertension in response to brain injury.
Stage 1- CSF production is reduced and constriction of blood vessels occurs Stage 2- failure of compensation (stage 1 doesnt work) pressure continues to rise, reducing oxygenation, increase in overall body blood pressure Stage 3- failure of brain autoregulation, brain opens up all of its main blood vessels (failure of autoregulation) causing an increase in blood volume in the brain and further increase in ICP Stage 4-ICP reaches level of systemic circulation blood pressure, pressures inside the cranial vault reach levels seen in systemic circulation, this results in brain herniation and complete shut down of oxygen delivery.
What are the 4 types if cerebral edema and their features?
1) vasogenic- clinically most important, increased permeability of capillary membrane after vascular injury, proteins leak into EC spaces drawing water, see severe increase in ICP 2) cytotoxic- toxic factors directly affect all cell types, active transport mechanisms lost, cells lose potassium and gain excess sodium, cells take in water and swell 3) ischemic- follows cerebral infarction, components of both vasogenic and cytotoxic, cells eventually undergo necrosis 4) interstitial- mostly in hydrocephalus, caused by movement of CSF from ventricles into EC spaces
What is the characteristic causative feature of hydrocephalus?
Refers to a variety of conditions characterized by excess fluid within the cranial vault, subarachnoid space or both
a reduction in normal power of one or more muscles
inability to sustain an activity
paralysis or plegia
indicate severe weakness that is complete or nearly complete
mild or moderate weakness
half of body
to both legs
to all four limbs
slight resistance of muscles to passive stretch or movement
increase in muscle tone
flaccidity or hypotonia
decrease in muscle tone
a visible or palable twitch within a single muscle
impaired relaxation after a contraction
excessive movement; several types
decreased movement (Parkinson's)
impaired ability to maintain the intended orientation or posture of the body in space
sudden, explosive, disorderly discharge of cerebral neurons
how is a seizure different from epilepsy?
epilepsy is a general term for the primary condition that causes seizures
Discuss general aspects of seizures
alteration in brain function usually involving motor, sensory, autonomic or psychic clinical manifestations as well as alterations in arousal; convulsion
What is a type I seizure?
partial seizure (seizures begin locally-entire brain isnt involved) a) simple (without impairment of consciousness) b) complex (with impairment of consciousness) c) secondarily generalized (partial onset evolving to generalized tonic-clonic seizures)
What is a type II seizure?
generalized seizures (bilaterally symmetrical and without local onset) absence, myoclonic, clonic, tonic, tonic-clonic, atonic, infantile spasms
What is a type III seizure?
What is a type IV seizure?
peculiar sensation preceding the onset of a partial seizure; gustatory, visual or auditory experience; feeling or dizziness or numbness
early clinical manifestation of malaise, headache, sense of depression; may occur hours to a few days before onset of a seizure
state of muscle contraction with excessive tone
state of alternating contaction and relaxation of muscles
shock-like muscular contractions
sudden loss of muscle tone
time period immediately following cessation of a seizure
derived from the Greek, epilepsia, meaning "to come upon, to be grabbed hold of or thrown down, to attack, to seize hold of". A condition in which a person has recurrent seizures due to a chronic, underlying process-it is a clinical phenomenon rather than a single disease entity
group of neurons demonstrating a paroxysmal depolarization due to sudden changed in membrane activity; originated from gray matter in any coritcal or subcortical area
small number of neurons initially involved
subsequent breakdown in normal membrane ion conductance and excitatory/inhibitory synaptic input occurs and the excessive excitability spreads
Which ion appears to be the primary one altered causing membrane instability; how does this result in the instability?
Membrane instability ay be due to altered potassim conductance as a result of increased extracellular K+, a defect in volatage-sensitive ion channels (increased Ca2+ and Na+ entry) and/or deficiency in membrane ATPases
Discuss what changes in GABA and glutamate may be occurring and how do they contribute to the altered neuronal excitabilty?
decreased GABA inhibitory and/or increased glutamate (NMDA) excitatory input may be involved (other excitatory and inhibitory NTs and NMs may be involved)
How is seizure activity maintained and ultimately how does this result in brain damage?
Maintenance of seizure activity depends on increased blood supply of nutrients and removal of carbon dioxide-cerebral oxygen consumption is increased 60% and ATP demand is increased 250%; blood flow increases 250% in an attempt to provide the necessary fuels, however, glucose and oxygen are rapidly depleted ( and ultimately ATP); the more prolonged the seizure the more likely the brain will suffer from ischemia resulting in neuronal destruction and brain damage due to hypoxia, acidosis, and lactate accumulation
Describe the tonic phase of a seizure
evidenced early in the seizure with muscle contraction and increased muscle tone-high level of excitability
Describe the clonic phase of a seizure
follows with alternating contraction and relaxation of muscles and increased inhibitory neuronal activity attempting to offset the excitation; eventually the epileptogenic neurons become exhausted
Define status epilepticus and list common causes
Any seizure lasting longer than 30 minutes (with or without impaired consciousness) or recurrent seizures without an intervention period or consciousness between seizures. primary causes in children is infection and metabolic disorders; primary causes in adults are cerebrovascular disease and anticonvulsant withdrawal
Discuss the speculated mechanism of status epilepticus
Alterations in GABA (levels ar einitially increased but this causes receptor endocytosis resulting in decreased inhibitory input) and glutamate (NMDA and AMPA receptors- increased Ca2+ and Na+ influx) appear to be involved; potential for free radical involvement
Differentiate between GCSE and NCSE
GCSE- generalized convulsive status epilepticus- most common presenting as repeated generalized seizures involving both hemispheres. NCSE- nonconvulsive SE "twilight" state with altered conscious and/or behavior
List and briefly describe the two types of stroke and what typically causes each?
1)ischemia with or without infarction- reduction in blood flow lasting several seconds to a few minutes 2)Cerebral hemorrhage- hypertension is primary cause, other causes are ruptured aneurysms, vascular malformations, bleeding tumor, bleeding disorders, head trauma
which type of stroke has the highest incidence?
what are the nonmodifiable risk factors/risk markers of ischemic stroke?
age, gender, race, family history of stroke, low birth weight
what are the modifiable, well documented risk factors of ischemic stroke?
hypertension, atrial fibrillation, other cardiac diseases, diabetes, dyslipidemia, cigarette smoking, alcohol, sickle cell disease, asymptomatic carotid stenosis, postmenopausal hormone therapy, obesity, physical inactivity, diet
what are the potentially modifiable, less well documents risk factors of ischemic stroke?
oral contraceptives, migraine, drug and alcohol abuse, hemostatic and inflammatory factors, homocysteine, sleep-disordered breathing
brain tissue will recover if have rapids restoration of blood flow- effects are transient (TIA); typically lasts 5-15 minutes, but by definition last <24 hours
With respect to time, at what point does an infarction typically occur?
cessation of blood flow for more than a few minutes will result in infarction-death of brain tissue
Define focal ischemia
focal ischemia or infarction is one caused by thrombosis or emboli; have a zone of cell loss surrounded by zone of injured cells (penumbra)
Define global ischemia
global hypoxia-ischemia occurs as a result of overall reduction in cerebral blood flow due to atherosclerosis and hypotension
Which neurotransmitter contributes to cell swelling following infarction?
cellular events include depletion of ATP leading to an increase in intracellular SODIUM resulting in cell swelling
Define a penetrating artery disease infarct
small cavity of fluid left after infarction; arterial hypertension closely related to occurrence; a key feature is that the arteries affected exhibit a lipohyalinotic thickening leading to occlusion
discuss events of the cascade of cerebral ischemia
ARTERIAL OCCLUSION 1) glutamate release 2) energy failure (loss or decrease in ATP) 3) Ca2+/Na+ influx 4) thrombolysis/thrombectomy 5) free radical formation 6) mitochondrial damage 7) inflammatory response 8) membrane and cytoskeletal breakdown
Describe a cerebral hemorrhage stroke with respect to extent, cause and type of edema
Starts out typically as focal neurologic deficit but ultimately involves a large area of tissue at site of hemorrhage. Hypertension is a primary cause; smaller arteries particularly susceptible. Mass of blood in brain displaces brain tissue producing additional ischemia in areas not initially affected causing vasogenic edema-ICP increases
Where do thrombi typically form in ischemic stroke and hat is the major underlying reason for the thrombus formation; what happens to the vessel wall to cause the clot formation.
Occurrence of thrombi likely in areas of plaque development where there is significant narrowing of the artery. Dehydration, hypotension, prolonged vasoconstriction (from hypertension) also increase the risk of thrombus formation. Ulcerated areas of the vessel wall form allowing platelet and fibrin to adhere resulting in clot formation
Describe an embolic stroke and what are the major causes?
Typically occur as a result of a thrombus breaking off and traveling to a distal vessel ultiamtely blocking blood glow (artery-to-artery stroke). Emboli can also from from an ulcerated atherosclerotic plaque, atrial fibrillation, MI, endocarditis, valvular prosthesis as well as air, fat or tumor cells
Describe the role of the various etiologic factors involved in IPD
-neurotoxins (MPTP/MPP) targeted to dopaminergic (DA) neurons in substantia nigra. -Oxyradicals, including metabolism of DA; loss of balance of oxidant/anti-oxidant mechanisms. -NO toxicity, inflammation, excitotoxicity, apoptosis, mitochondrial and proteosomal dysfunction, autophagy
What neurotransmitter and its pathway is altered in IPD; discuss the pathophysiologic features of this disease.
Hallmark change is loss of dopaminergic projections from the substania nigra and striatum; DA normally acts on D1(direct pathway) and D2 (indirect pathway) receptors in the striatum which mediate two separate pathways to regulate cortically controlled environment. During the time of progressive loss there appears to be up-regulation of DA synthesis and down-regulation of reuptake to compensate for loss of neurons. In IPD the loss of DA in the substantia nigra results in decreased activation of the cortex.
How does excess cholinergic activity occur in IPD and what are the consequences
excess cholinergic activity in striatal interneurons probably accounts for the tremors observed in IPD; the excess cholinergic activity results from loss of inhibitory actions of DA on cholinergic neurons
Discuss the clinical presentation of an IPD patient
primary are limb muscle rigidity, resting tremor(usually first symptom) abolished by movement, bradykinesia, postural instability. Although predominately a disorder of motor capabilities neuropsychological abnormalities may be seen- dementia and affective disorders increased. Insidious development, progressively worsens, but may remain stable for years
list the 4 general clinical features of IPD
resting tremor, rigidity, bradykinesia, postural instability (difficulty with maintaining balance)
Identify motor symptoms of an IPD patient
decreased manual dexterity, difficulty arising from seated position, diminished arm swing during ambulation, dysarthria (slurred speech), dysphagia (difficulty with swallowing), festinating gait (tendency to pass from a walking to a running pace), flexed posture (axial, upper/lower extremities), "freezing" at initiation of movement, hypomimia (reduced facial animation), hypophonia (reduced voice volume), and micrographia (diminution of handwritten letters/symbols)
Identify autonomic symptoms of an IPD patient
experience bladder and anal sphincter disturbances, diaphoresis, fatigue, olfactory disturbance, othrostatic blood pressure changes, pain, pareshesia, paroxysmal vascular flushing, seborrhea, sexual dysfunction, and sialorrhea (drooling)
Identify the mental status changes of an IPD patient
experience anxiety, apathy, bradyphrenia (slowness of thought process), confusional state, dementia, depression, hallucinosis/psychosis (typically drug induced), and sleep disorders
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