unit 3 patho

what are nociceptors

free nerve endings located in skin, muscles, joints, and internal organs that respond to mechanical, thermal and chemical injury

how do nociceptive signals travel

via the peripheral sensory neurons to the dorsal horn of the spinal cord then ascend to higher brain centers - thalamus and cerebral cortex

somatic pain vs visceral pain

somatic pain (nociceptive) is in the skin, muscles, bones, and joints and is typically well localized, visceral pain is in the internal organs and is poorly localized and associated with autonomic symptoms like nausea and sweating

why do we feel pain during the inflammatory process

inflammatory mediators sensitize nociceptors which lowers their activation threshold amplifying pain which contributes to tenderness and hyperalgesia

what is neuropathic pain

injury/dysfunction of the somatic nervous system rather than tissue damage - peripheral nerves, spinal cord pathways, central pain processing regions. all of which leads to abnormal signaling, which is described as shooting, electric, or burning pain; typically chronic and maladaptive

what is central sensitization

repetitive or intense nociception leading neurons in the spinal cord and brain to become hyper responsive resulting in exaggerated pain responses

what could cause heightened pain sensitivity

dysfunction of modulatory systems (those that release NTs like serotonin, norepinephrine, and endogenous opioids)

what could alter pain processing

many disorders alter pain processes

• neuro - spinal cord injury, MS causing neuropathic pain

• CNS disorders - stroke and traumatic brain injury causing central pain syndromes due to altered cortical and subcortical processing

• headache disorders - migraines reflecting complex interaction of neural excitability and vascular changes

what is episodic pain

pain that is recurrent yet not constant - flare ups or attacks accompanied by pain free periods (migraines, kidney stones, or angina); often associated with long term medical conditions

what is nociplastic pain

pain arising from altered nociception without clear evidence of tissue injury or nerve damage; often widespread and associated with fatigue and poor sleep (fibromyalgia, IBS)

nocicpetion vs pain

nociception - neural process of responding to stimuli which occurs with or without awareness, pain - subjective experience influenced by emotion and environment. Someone can experience nociception without pain (anesthesia) and pain without nociception (phantom limb)

referred pain is

felt in another area than origin because of a shared nerve pathway (heart attack felt in left arm/jaw, gallbladder pain being felt in right shoulder)

what are some treatment options for pain

nociceptive - NSAIDs, PT, activity modification

neuropathic - drugs that target brain like gabapentin and antidepressants

nociplastic - alleviate anxiety with stress management, sleep hygiene

first step of pain signaling is

transduction - nociceptors are activated by harmful stimuli and convert it into electrical signals; influences by inflammatory mediators (cytokines - central sensitization)t

what is the second step of pain signaling

transmission - signal is carried to spinal cord through peripheral sensory neuron then the second order neuron (dorsal horn of spinal cord); info is taken up spinal cord and into brain, travels through white matter of spinothalamic tract; synapses on third order neuron - thalamus out to cortex (somatosensory) where signal is interpreted

what is the third step of pain signaling

perception - pain becomes conscious experience; brain interprets intensity, location, and emotions (somatosensory and limbic systems)

what is the fourth step of pain signaling

modulation - process of amplifying or dampening pain signals. Descending pathways release natural opioids and other chemicals to reduce pain which excitatory NTs can amplify pain (endorphins, epinephrine)

what is delirium

acute confusional state characterized by a sudden onset of fluctuating levels of consciousness, impaired attention, and disorganized thought processes; may develop rapidly

what is a supratentorial alteration of arousal

located above tentorium cerebelli; produces changed by either diffusing or localized dysfunction

what is an infratentorial alteration of arousal

below tentorium cerebelli (gap between parietal and occipital lobes); destruction of reticular activating system (regulations behavior and consciousness) and destruction of brain stem

what is a metabolic alternation of arousal

alteration of energy delivery - hypoxia, electrolytes (potassium, sodium), and hypoglycemia

what are psychogenic alterations of arousal

uncommon yet can present in psychiatric disorders; despite apparent unconsciousness the person is physiologically awake and neurologic exam reflects normal responses

what are 5 critical evaluations of consciousness

level of consciousness (most critical), pattern of breathing, pupillary reaction, oculomotor responses, motor responses (can determine which side of brain)

when does brain death occur

brain is no longer able to maintain homeostasis - unresponsive coma, no spontaneous respiration, no brainstem function, flat EEG, persistence of signs for appropriate period of time (*must not be caused by depressants, hypothermia etc*)

symptoms of cerebral death

difficulty speaking and seizures - caused by hypoxia and is usually irreversible. brainstem may continue to function

what will survivors of cerebral death experience (think of comfort patients)

remains in coma with eyes closed and will not follow commands; may progress into vegetative or minimally conscious state. Individual’s eyes may open spontaneously, BP and breathing are maintained without support, bowel and bladder incontinence (recovery is unlikely)

seizures are

sudden, transient alteration of brain function caused by abnormal excessive discharges of cortical neurons often leading to convulsions

what are associated conditions with seizures

metabolic disorders, congenital malformation, perinatal injury, myoclonic syndromes, infection, tumors, vascular disease, and substance use

how do we classify seizures

dependent on area of abnormal discharge and origin site; EEG will correlate; can be focal (originate in one area of brain) or generalized (affect more than one area of brain typically on both sides at the same time)

what are precipitating factors that may trigger a seizure

fever, fatigue, stress, metabolic or hormone changes, drug/alcohol use, odors, flashing or strobe lights, skipping medication, dehydration

what is the preictal phase

prodroma symptoms before seizure occurs - aura (unusual sensory experience)wS

what is the ictus phase

the actual seizure

what happens during postictal phase

headache, confusion, deep sleep, dysphasia, memory loss, and paralysis

what is staticus epilepticus

state of continuous seizures that are very close together and will not stop without treatment

what is the root cause of delirium

disruption of brain networks rather than discrete area - metabolic disturbance like hypoglycemia and thyroid disorders; UTIs, electrolyte imbalances - interfere with neuronal metabolism or synaptic transmission

how does delirium initally manifest

restlessness, irritability, difficulty concentrating, insomnia, tremulousness, and poor appetite (some may experience seizures)

what are the mechanisms of dementia

neuron degeneration, brain tissue compression, atherosclerosis, brain trauma, and infection/neuroinflammation

what are pathologic alterations of Alzheimer’s

neurotic plaques and neurofibrillary tangles causing loss of brain function

how do we treat parkinsons

drug therapy but cannot be started until symptoms are incapacitating due to side effects and loss of effectiveness overtime

where is genetic defect of huntingtons

autosomal dominant trait on chromosome 4 contains an abnormally long polyglutamine tract in the huntingtin protein that is toxic to neurons (50% chance of inheritance)

what are the symptoms of HD

involuntary hyperkinetic movement such as chorea (jerky, abnormal movement in the face and arms that eventually affects the entire body), athetosis, and ballism

how does ALS involve upper and lower motor neurons

amyotrophic (progressive muscle wasting) refers to lower motor neuron component while lateral sclerosis refers to upper motor neuron caused by scarring of the pyramidal (corticospinal) tract

what do we use to treat cerebral edema

oxygen, osmotherapy, diuretics, CSF drain tube, maintenance of BP thru fluid management, steroids

what is hydrocephalus

excess fluid in cerebral ventricles or subarachnoid space caused by interference of CSF flow; leads to increased fluid production, obstruction in ventricles, defective reabsorption

what is noncommunicating hydrocephalus

internal - buildup of CSF in brain causing ventricles to widen harming tissue

intraventricular - inside or around ventricles, spaces normally containing CSF

communicating hydrocephalus

occurs when CSF can flow freely within ventricles yet is not absorbed properly

acute hydrocephalus

present with signs of rapidly developing intracranial pressure; person will quickly develop into coma without removal of fluid

normal pressure hydrocephalus

dilation of ventricles without an increase in pressure, may notice decline in memory and cognitive function - unsteady gait, history of falls, incontinence, and dementia

what is herniation

displacement of brain tissue compressing other parts

what is uncal herniation

life threatening condition when uncus (part of temporal lobe) moves due to lesions and compresses brainstem; most common

what is subfalcine herniation

disease in frontal, parietal, or temporal lobe on one side of the brain that increases intracranial pressure and pushes cingulate gyrus under falx cerebri

what is tonsillar herniation

condition where the cerebellar tonsils move downward through foramen magnum

what is amnesia

retrograde or anterograde - retrograde involving the loss of previously formed memories and anterograde involving the inability to form new memories; associated with injury to hippocampus and limbic structures

what is aphasia

language disturbances that occur when damage to cortical regions of the brain occur; individuals may experience difficulty forming speech, understanding spoken or written language, or both; often associated with CVAs in the dominant cerebral hemisphere

what is agnosia

inability to recognize objects, people, sounds, or smells despite intact sensory pathway; occurs due to disruption of higher order pathway in parietal, temporal, and occipital lobes

what is associated with interstitial edema

CSF obstruction resulting in increased intercranial pressure - acute hydrocephalus

what is associated with vasogenic edema

increased permeability of capillary endothelium of brain after injury; primarily in white matter

what is associated with cytotoxic edema

failure of Na/K pumps and loss of gradient; causes osmosis into cells resulting in cell swelling - from brain injury or ischemia, hypoglycemia, and hypoosmotic states that impair sodium potassium pumps

what is the significance of CPP (cerebral perfusion pressure)

difference between mean arterial pressure and intracranial pressure. CPP is the driving force of cerebral blood flow

ischemic vs hemorrhagic stroke

ischemic - cerebral artery is obstructed by thrombus or embolus leading to tissue ischemia and infarction

hemorrhagic - rupture of blood vessel causing blooding into or around brain leading to rise of ICP

what is a transient ischemic attack

temporary reduction in cerebral flow with symptoms that resolve within 24 hours - increase risk of future stroke

upper motor neuron syndrome

originate in motor cortex and descent through brainstem/spinal cord to synapse on lower motor neurons - syndrome reflects loss of inhibitory control over spinal reflexes rather than direct muscle devernation (spastic weakness, increased muscle tone, hyperreflexia, clonus)

lower motor neuron syndrome

extend from anterior horn of spinal cord or cranial nerve nuclei directly to skeletal muscle fibers; characterized by flaccid weakness, decreased/absent reflexes, hypotonia, and muscle atrophy - leads to loss of muscle mass

what do disorders of the extrapyramidal motor system cause

system includes basal ganglia and associated pathways, typically regulates movement initiation, posture, muscle tone, and smooth execution of voluntary motion - disorder would produce abnormal movements and changes in muscle tone

what is included in drug therapy for parkinsons

dopamine agonists, anti-tremor, and antidepressants

what is the pathophysiology of HD

degeneration of basal ganglia leading to depletion of GABA which alters integration of motor and mental function

what is the pathophysiology of MS

develops from previous viral infection/pregnancy/infection that causes inflammation and demyelination of the axons leading to irreversible degeneration and scarring - injury is caused throughout CNS leading to MS lesions (requires genetic predisposition)

what are the 4 types of MS

remitting relapsing - disease relapses and remits - symptoms become worse and then improve

primary progressive - disease continually progresses

secondary progressive - progression comes after relapsing remitting

progressive relapsing - progressive worsening from beginning (least common)

what are diagnosing factors of MS

no exact diagnosis - many show IgG antibodies in CSF, can combine with MRI results

how do we treat MS

prevent exacerbation and permanent neurological damage; drugs include corticosteroids, immunosuppressants, and immune modulators

what is guillian-barre

immune mediated demyelination of peripheral nerves causing weakness, parasthesis, and paralysis; following viral or bacterial infection resulting from abnormal immune response targeting peripheral nerve myelin - primarily in LMN

what is tabes dorsalis

rare sever complication of tertiary syphilis, very rare; demyelination of posterior roots/columns of spinal cord causing sensory deficits; produce gummas on skin

what is myasthenia gravis

disorder of NMJ caused by autoimmune destruction/blockage of ACH receptors on post synaptic muscle membrane - neuromuscular transmission is inefficient resulting in fluctuating muscle weakness (commonly affects eye movement, facial expression, chewing, swallowing, and speaking)

differentiate primary vs secondary injury

primary injury is at moment of impact while secondary injury is later and arises from cerebral edema, increased intracranial pressure, ischemia, inflammation, and excitotoxic NT disease