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164 Cards in this Set

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What are the basic mechanisms of headaches?
increased intracranial pressure (tumor or hemorrhage); vascular distention and dilation (esp. arteries); inflammation of mucosal structures, nasal sinuses, meninges, or perivascular areas; sustained contraction of skeletal m. of scalp and neck
Does the brain parenchyma itself produce pain?
What are the four types of vascular headaches?
migraine with aura (classical migraine); migraine without aura (common migraine); cluster headache; complicated migraine (hemiplegic, opthalmoplegic; basilar types)
What are the symptoms of a classical migraine?
an aura or prodrome of flashing or scintillating lights, visual loss, aphasia, severe, throbbing unilateral pain; poor light or sound tolerance; autonomic symptoms (sweating, nausea, vomiting, dizziness); headache and malaise can last 1-2 days, onset in teens or twenties
What is a primary headache versus a secondary headache?
primary: the headache is the key; secondary: the headache is a result of tumor or trauma
Who normally gets classical migraines?
more common in women and frequently there is a family history; indivual has no other red flags on H/P to suggest another cause of the pain
What are the symptoms of a common migraine?
no visual prodrome (aura) but possibly illness prior to onset of headaches; severe, throbbing unilateral pain; poor light or sound tolerance; autonomic symptoms (sweating, nausea, vomiting, dizziness); headache and malaise can last 1-2 days; more common in women
What are the symptoms of a cluster headache?
severe headache for a short duration (2-3 hrs); occuring in a cluster of days or weeks, with long periods of remission; periorbital pain (unilateral boring), ipsilateral red, watery eye, nasal discharge and congestion, transient Horner's syndrome, pt. paces restlessly during headache
Who normally gets cluster headaches?
What are the symptoms of a complicated migraine?
hemiplegia, extraocular muscle palsy, other brainstem symptoms
What are the two possible mechanisms of migraines?
vascular reactivity; trigeminovascular theory
How can vasoactivity cause migraine symptoms?
vasoconstriction of occipital arteries can cause the visual prodrome; vasodilation of extracranial arteries can cause a throbbing headache; thus vasoactive drugs can worsen (nitrogycerin) or relieve (ergotamine) the migraine
What is the trigeminovascular theory of migraine mechanism?
Serotonergic neurons (raphe)/ or NE from cereleus trigger vasodilation of extracranial arteries which is perceived as pain by the perivascular trigeminal afferents and cause nausea, vomiting; the trigeminal afferents antidromically (in reverse) release substance P at vascular sites leading to neurogenic inflammation
What are the treatments of migraine?
relaxation; avoiding triggers; nonspecific drugs (analgesics, antiemetics, sedatives, NSAIDs); specific drugs to abort attack (ergot alkaloids ie.DHE, sumatriptan); specific drugs to prevent attack (β adrenergic blockers (propranolol); Ca channel blockers; methysergide; tricyclic antidepressants; valproate) often exert effects on serotonin receptors
Where do many of the drugs in treating migraine exert their effects?
serotonin receptors
What are types of headaches other than migraine?
muscle contraction (tension); combined (vascular and muscle contraction); traction (after LP); pseudotumor cerebri; meningitis; temporal arteritis; trigeminal neuralgia; infection or allergy of eye, ear, nose, sinus, teeth
What are the characteristics of a tension headache?
most common variety; causes steady pressure or band, with hours to day-long duration, little autonomic involvement; often related to stresses or depression; possibly due to muscle contraction of neck, scalp and shoulders; may improve with tricyclic antidepressants or antiinflammatories
What are the characteristics of a traction headache?
resulting from a lumbar pucture due to decreased CSF; relieved when lying down flat; epidural blood patch is most effective therapy to stop the dural CSF leak
What are the characteristics of a pseudotumor cerebri headache?
migraine-like headache often in obese; due to increased intracranial pressure resulting in papilledema and other tumor-like symptoms; acetazolamide or shunt procedure to relieve pressure and prevent blindness
What are the characteristics of a temporal arteritis headache?
often in elderly, achy muscles, weak fatiguable chewing, visual blurring, low grade fever, anemia, polymyalgia, often due to inflammation of the temporal nerve; treat with corticosteroids to prevent blindness
What are ominous headache symptoms?
severe headache without prior history; sudden or progressive worsening of chronic headache; awakens pt. from sleep; associated seizure or loss of consciousness; memory disturbance, personality change, neurological deficit
Which type of brain scan is most appropriate for an unstable trauma patient with abdominal bleeding, headache, and lethargy?
CT-scan, because it is quick and hemorrhage is easily detected by it
A young woman with optic neuritis has had previous episodes of ataxic gait and tingling legs. Which types of brain scan is most helpful in her evaluation?
brain MRI is more sensitive in demonstrating white matter plaques (MS best seen with T2W or FLAIR)
A severely disabled child has had medically uncontrollable seizures since birth. Which type of brain scan might localize the seizure focus for surgical resection?
A PET, SPECT, or fMRI performed during a seizure may show what cortical area originates the seizure
What scan provides images of cerebral arteries without inserting a catheter or injecting iodinated contrast?
MRA noninvasively images cerebral arteries but not as well as a conventional angiogram
What kinds of procedures are done with interventional angiography?
place coils into inoperable cerebral aneurysms or vascualr malformations via intraarterial catheters to prevent hemorrhage when they thrombose, reexpand stenotic arteries with balloons or stents, thrombolytic agents selectively injected into recently occluded arteries;
What does intravenous iodinated contrast used with CT scan do to images?
opacifies or gives greater density to normal vascular structures and brain lesions that have a breakdown of the BBB surrounding them (ie. recent infarcts, tumors, or abcesses)
What are the advantages of CT?
rapid scanning time (for very sick, unstable, uncooperative pts); less affected by motion artifact (moving pts); readily detects fresh hemorrhage; good method for evaluating skull bones
What are the disadvantages of CT?
bony artifact impairs visualization of posterior and temporal fossae; pt. needs to be repositioned in scan to see different planes; radiation exposure; side effects to IV iodinated contrast; intrathecal contrast to image the spinal cord
What are T1 weighted MRIs best for imaging?
highlighting anatomy (CSF is dark)
What are T2 weighted MRIs best for imaging?
highlighting pathology (CSF is bright)
What are FLAIR (fluide attenuation recovery) MRIs best for imaging?
highlighting pathology like T2 but removes the visually distracting bright signals of CSF
What color are vessels with flowing blood on MRI? Why?
dark or no MRI signal because the protons flowing in the blood leave the plane being imaged before emitting a signal. Thrombosed vessels show an increased signal because they lack this flow of blood
What are the advantages of MRI?
highest resolution images of brain and spinal cord; detects pathology often missed on CT (demyelination, inflammation, mets); not affected by bony artifact (see posterior and temporal fossae); can create sagittal and coronal planes without repositioning the pt, no radiation exposure; iodinated contrast not used
What are the disadvantages of MRI?
slow scanning time; sensitive to motion artifact; metallic objects are unsafe in the magnetic field; claustrophobia of pts
What is an MRA (magnetic resonance angiography)?
a scan to image arteries and veins based on the behavior of blood flowing through the magnetic field, no catheter injection is needed so is safer and less invasive than an angiography; angiography gives better resolution
What scan is best to image acute infarction?
MRI, able to see even small infarcts, DWI (bc water diffusion is impaired in ischemic brain); T2W, and FLAIR (are high signal)
What are characteristics of a primary brain tumor?
solitary lesion, irregular shaped, hemorrhagic, and heterogeneous
What are characteristics of a metastatic brain tumor?
solitary or multiple, spherical shape, often located in gray-white matter junction
A teacher has had 2 weeks of back pain radiating down his posterior left leg. Which scan might readily show a herniated disc? What if he has a cardiac pacemaker?
lumbar spine MRI images spondilosis, herniated disk, and spinal stenosis best; however with a cardiac pacemaker a CT myelogram (uses injection of contrast into intrathecal space) can be done
What is a seizure?
an excessive high-frequency discharge of cortical neurons in the brain
What is epilepsy?
the recurrence of seizures from a hyperexcitable focus of cortex near the glial scar of prior injury or resulting from global disinhibition of neurons, the focus often shows a prominent spike on EEG
What are the normal mechanisms to prevent excessive depolarization of the neuronal membrane?
hyperpolarization by IPSPs from inhibitory interneurons; uptake of K by astrocytes during APs, long electronic length of neurons so that dendritic excitation is distant from the axon hillock where APs are initiated
What causes seizure initiation?
cortical neurons, esp. pyramidal neurons, that fire repetitively in short high-frequency burst of APs from a paroxysmal depolarization shift
What is seizure generalization?
when normal brain regions are recruited into epileptic activity, esp due to the local circuit involvement of layers 2 and 3 of the cortex which spread the signals to other regions in the cortex, also subcortical structures such as the basal ganglia transmit the activity to other regions.
What are the four types of clinical seizures?
simple partial seizure, complex partial, generalized nonconvulsive (absence), generalized tonic-clonic seizure
What are the characteristics of a simple partial seizure?
localized cortical involvment initiates rhythmical, involuntary tonic-clonic jerking of face, arm, leg on one side or localized sensory, visual or autonomic disturbance; without loss of consciousness, pt is able to recall the event, and there is no postictal state
What are the characteristics of a complex partial seizure?
unresponsiveness, sometimes with automatisms or repetitive semipurposeful events; causes impaired consciousness and amnesia of the event, postictal confusion; often localized to medial temporal lobe (hippocampus and amygdala)
What are the characteristics of a generalized, nonconvulsive seizure (absence)?
brief impairment of consciousness (few seconds), followed by resumption of previous activity, no postictal confusion, occurs in childhood and outgrown, EEG shows typical 3/sec spike and slow wave bilateral, generalized discharge
What are the characteristics of a generalized, tonic-clonic seizure?
bilateral, vigorous, rhythmic, tonic-clonic contractions of body muscles with loss of consciousness and amnesia; postictal confusion; possibly resulting from spread of simple or complex partial seizure or diffuse global discharge
What are symptoms preceding a generalized tonic-clonic seizure?
vague dizziness and nausea, aura (tingling or twitching of an arm which is actually the beginning of the seizure and can help localize the focus)
What are symptoms during a generalized tonic-clonic seizure?
tonic phase: contraction of muscles (causes falling, expel air), loss of consciousness, apnea causing cyanosis; clonic phase: rhythmic, forcible twitching, tongue biting or oral trauma, excessive salivation; Postictal: rapid breathing, confusion and sleepiness, incontinence
What are the causes of primarily generalized seizures?
global, synchronous cortical discharges; diffuse cortical disinhibition; diffuse permanent brain injury (anoxia, metabolic disorder, brain malformation); transient metabolic disorder (drugs, drug withdrawl, toxins, electrolyte disturbance)
What are the causes of secondarily generalized seizures?
focused cortical discharge site due to trauma, infection/inflammation, stroke, tumor; cortical generalized spread precipitated by sleep deprivation, systemic illness, stress, alcohol
What diagnostic tests are done for seizures?
EEG (record brain wave activity due to summated synaptic activity); CT, MRI to identify infarts, tumors, or hemorrhage; Lumbar puncture to exclude encephalitis or meningitis
What are some treatments for seizures?
general: protect convulsing pt, maintain airway; monitor/treat hypoglycemia, infections, HTN; anticonvulsant drugs one at a time (inactivate neuronal Na channels: carbamezepine, phenytoin, valproate) or (potentiate GABA inhibition: benzodiazepines and phenobarbital); surgery to resect causative cortex
What is status epilepticus?
continued, unabated seizure or repeated seizures for 30 minutes or longer; is an emergency that can cause brain damage, metabolic disorders, and respiratory arrest; treat with benzodiazepines (diazepam) followed by longer acting anticonvulsants
What are the clinical features of coma?
a sleeplike unarousable unresponsive state, only able to test brainstem reflexes bc. Cortical function is lost
What are pathogenic causes of coma?
severe metabolic or systemic conditions that diffusely depress cortical function (hypoxia, hypoglycemia, electrolyte imbalance, infection, hepatic/renal failure, drug overdose); bilateral or diffuse cerebral lesions (encephalitis, meningitis, hemorrhage, infarct, tumor); brainstem lesions disrupting the reticular formation
How does one examine an unresponsive patient?
breathing patterns, pupil size and reactivity, reflexive ocular movements, motor responses
What types of breathing patterns are seen in coma patients?
cheyne-stokes respiration; central neurogenic hyperventilation; ataxic respiration
What is cheyne-stokes respiration and who can have it?
alternating hyperpnea and apnea; occurs with healthy sleeping eldery; CHF (bc prolonged circulation time); metabolic encephalopathies (renal failure); bilateral cortical structural lesions
What is central neurogenic hyperventilation and who can have it?
persistently deep, rapid respirations; usually reflexive response to severe pulmonary congestion; lesion or edema in the low midbrain to upper pons
What is ataxic respiration and who can have it?
completely irregular respiration; lesion or edema in the medulla (location of cardiopulmonary control centers), may signal impending respiratory arrest
Is the pupillary light reflex usually preserved in metabolic or structural causes of coma?
What does a midbrain lesion do to the pupils?
tectal midbrain lesion selectively involves the parasympathetic fibers causing large, fixed pupils bilaterally (unopposed sympathetic fibers)
What does a very large, fixed (blown) pupil indicate?
compression of the ipsilateral CN III from a swollen temporal lobe (uncal herniation)
What does a pontine lesion do to the pupils?
selectively involves the sympathetic fibers of the hypothalamo-autonomic fibers, causing small, pinpoint pupils (unopposed parasympathetic fibers)
Does asymmetrical abnormalities in eye movements or pupils more likely represent a metabolic or structural cause of coma?
What is the oculocephalic reflex?
doll's eyes, the eyes should normally move in the direction opposite to the lateral turn of the head (brainstem reflex) in a comatose pt. If they vixate some cortical function is involved
What is the oculovestibular reflex?
cold caloric reflex, irrigation of ear with ice water reduces the ipsilateral semicircular canal activity and causes eyes to move toward the irrigated ear if the brainstem is intact
What is decorticate posturing?
flexion of upper limbs extension of lower limbs; caused by lesion at the cortical or hemispheric level
What is decerebrate posturing?
extension of upper and lower limbs; caused by a lesion at the level of the midbrain (red nucleus)
What are the emergency treatments for all comatose patients?
establish respiration, oxygenation, circulation; rule out hypoglycemia
What is symptomatic of a metabolic coma?
symmetrical signs
What is symptomatic of a structural coma?
asymmetrical signs and/or history of head trauma
What are the emergency treatments for metabolic comatose patients?
exclude electrolyte abn, hypothermia, hepatic or renal failure; check drug screen (give narcotic or benzodiazepine antagonists); rule out subarachnoid hemorrhage, meningoencephalitis (CT or LP)
What are the emergency treatments for structural comatose patients?
CT or MRI to exclude hemorrhage, infart, or mass lesion; treat brain edema, surgery
What are the clinical criteria for declaration of brain death?
the cause is known and of sufficient severity to cause irreversible coma; adequate treatment of the cause without improvement; no drug intox, circulatory shock, hypothermia; brainstem and cerebral death findings persist beyond 6 hours
What are the signs and symptoms of brain death?
no spontaneous or induced movement initiated by rostral centers (decorticate, decerebrate posturing, seizures, swallowing, yawning, vocal); no pain-induced limb movement, no CN or brainstem reflexes, no spontaneous respirations (apnea test); sometimes presence of spinal mediated responses
What are ancillary tests of cerebral function?
EEG, radioisotope brain scan (to observe intracranial blood flow) preferred test for brain death
What is the postictal phase and its significance?
period of confusion that follows a complex partial or generalized tonic-clonic seizure. Simple partial, absence, or syncope (fainting) do not have postictal states)
What are the two requirements to determine brain death?
1. clinical brain death (by exam of the patient); 2. confirmatory tests (radioisotope brain scan, or EEG)
If a patient lacks a corneal response, where is the lesion?
pontine (lacks CN V and CNVII)
What reflexes will a patient lack if they have a lesion at the ponto-medullary junction?
no doll's eyes, no response to cold caloric testing
What are the two main parts of consciousness and what controls each?
Content: Limbic controls mood, attention, integration, cathexis; Cerebral controls perception, awareness, language, motor, planning; Arousal: controlled by brainstem
What reflexes will a patient lack if they have a lesion in the medulla?
cough and gag reflexes, CN IX and X; perform apnea test if no respiratory effort with pCO2 over 60 on 100% O2 the medulla is affected
What are the three parasagittal zones of the hypothalamus?
lateral (medial forebrain bundle); lateral (all the defined hypothalamic nuclei); periventricular gray
What are the four rostrocaudal levels of the hypothalamus?
preoptic, supraoptic, tuberal, and mammillary levels
What is the medial preoptic area (MPOA) of the hypothalamus related with?
sexual dimorphism (larger in males than females); sexual arousal (increased neuronal activity here in males, decreased in females); gonadotropin releasing hormone (GnRH) cells; fever and body temperature regulation
What four nuclei are within the supraoptic level of the hypothalamus?
paraventricular nucleus, suprachiasmatic nucleus; anterior nucleus; supraoptic nucleus
Where does the medial division (parvocellular) of the paraventricular nucleus of the hypothalamus project?
to the median eminence to secrete releasing or inhibiting hormones in the hypothalamo-hypophyseal portal system to the anterior pituitary to control autonomics, feeding etc.
Where does the intermediate magnocellular division of the paraventricular nucleus of the hypothalamus project?
directly to the posterior pituitary where oxytocin and vasopressin (ADH) are released directly into the circulation
What is the suprachiasmatic nucleus of the hypothalamus associated with?
acts as the master biological clock controlling various circadian and circannual rhythms, set to light-dark cycle by direct retinal projections, affected by jet lag
Where do the efferents and afferents of the lateral division of the paraventricular nucleus of the hypothalamus project?
efferents: solitary nucleus, dorsal motor nucleus of X, sympathetic preganglionic neurons of IML of lateral horn; afferents: (noradrenergic) solitary nucleus, ventrolateral medulla, locus ceruleus; and others from hypothalamic nuclei and limbic system
Where does the supraoptic nucleus of the hypothalamus project?
directly to the posterior pituitary where oxytocin and vasopressin (ADH) are released directly into the circulation; lesions here cause diabetes insipidus due to reduced ADH
What four areas/nuclei make up the tuberal level of the hypothalamus?
lateral hypothalamus, ventromedial nucleus; dorsomedial nucleus; arcuate nucleus
What does the lateral hypothalamus control?
synthesizes hypocretin (orexin) a neuropeptide involved in appetite and sleep regulation; lesions here reduce appetite
What does the protein leptin control?
produced in adipose tissue, it exerts a negative feedback on hypothalamus to control body weight
What are the afferents and efferents of the ventromedial nucleus of the hypothalamus?
afferent: amygdala via the stria terminalis; efferent: median eminence contributing to control of the anterior pituitary
Where does the arcuate nucleus of the hypothalamus project?
median eminence and hypothalamo-hypophyseal portal system contributing to control of the anterior pituitary; secretes more than one releasing hormone
What two nuclei make up the mammillary level of the hypothalamus?
mammillary nuclei, posterior nucleus
What are the afferents and efferents of the mammillary nuclei of the hypothalamus?
afferent: hippocampus via the fornix; efferent: brainstem reticular formation via the mammillotegmental tract, and anterior nuclei of the thalamus via the mammillothalamic tract
What two nuclei project into the posterior lobe (neurohypophysis) of the pituitary?
paraventricular nucleus and supraoptic nucleus
Where is the embryonic origin of the anterior lobe (adenohypophysis) of the pituitary?
roof of the embryonic oral cavity (not the neural tube)
What are the general functions of the hypothalamus?
integrating center concerned with autonomic, endocrine, visceral and limbic functions to maintain a stable internal milieu (homeostasis)
What is the function of the mammillary bodies?
involved with spatial learning and memory, sense head position in space and are highly interconnected with the hippocampal formation
What functions does the hypothalamus coordinate?
homeostatic functions: energy and fluid balance, thermoregulation, stress responses, circadian rhythm, sleep and arousal; Appetitive functions: reproduction, feeding, sleep, sickness
What clinical conditions are related to the hypothalamus?
obesity/anorexia/cachexia; fever; depression/anxiety; infertility/precocious puberty/delayed puberty; growth retardation; sleep disorders
What does the circle of willis circle?
the hypothalamus - highest blood perfusion rate of any tissue in the body
What are the unilateral (non-reciprocal) connections of the hypothalamus?
hypothalamohypophyseal tract (to pituitary); retinohypothalamic tract (from retina)
What is the hypothalamic origin, the name of the hypothalamic releasing or inhibiting hormone, and the hormone released from the Corticotroph cells of the anterior pituitary?
paraventricular nucleus (sress responses); +cortiotropin releasing hormone (CRH); adrenocorticotropic hormone (ACTH)
What is the hypothalamic origin, the name of the hypothalamic releasing or inhibiting hormone, and the hormone released from the Lactotroph cells of the anterior pituitary?
Medial tuberal nuclei (milk production); - Dopamine/+ Prolactin releasing factor; Prolactin
What is the hypothalamic origin, the name of the hypothalamic releasing or inhibiting hormone, and the hormone released from the Gonadotroph cells of the anterior pituitary?
continuum beginning just anterior to preoptic area; + Gonadotropin releasing hormone (GnRH); Luteinizing hormone (LH)/Follicle stimulating hormone (FSH)
What is the hypothalamic origin, the name of the hypothalamic releasing or inhibiting hormone, and the hormone released from the Somatotroph cells of the anterior pituitary?
arcuate nucleus / periventricular nucleus; + growth hormone releasing hormone (GHRH)/- Somatostatin; Growth hormone (GH)
What is the hypothalamic origin, the name of the hypothalamic releasing or inhibiting hormone, and the hormone released from the Thyrotroph cells of the anterior pituitary?
paraventicular nucleus; + thyrotropin releasing hormone (TRH); thyrotropin
What is the hypothalamic origin, the name of the hypothalamic releasing or inhibiting hormone, and the hormone released from the Melanotroph cells of the anterior pituitary?
MIF/MHSF; melanocyte stimulating hormone
What does the paraventricular nucleus of the hypothalamus control?
most important hypothalamic cell group regulating autonomic function, major source of input to intermediolateral cell column (sympathetics) and medullary parasympathetic cell groups
What is the sexually dimorphic nucleus of the hypothalamus?
preoptic nucleus
How are GnRH and gonadotropins released in males versus females?
males: pulsatile; females: surge
What is Kallmann's syndrome and its cause?
hypogonodotropic hypogonadism with anosmia - caused by the failure for the GnRH neurons to migrate along the nervus terminalis, due to a mutation in anosmin, a cell adhesion molecule, the GnRH neurons do not migrate from olfactory placode to forebrain, X-linked mutation
What is the mechanism for fever production in the medial preoptic area of the hypothalamus?
bacterial toxins (lipopolysaccharide or LPS), IL-1β, NE induce the gene for COX-2 in capillaries which produces prostaglandins E2 these activate MPOA neurons to activate heat production mechanisms (ie. shivering, no sweating, vasoconstriction) to cause fever
What behaviors of sickness behavior are coordinated by the hypothalamus?
sleep, food aversion, social isolation, fatigue/malaise, hypersensitivity to light/sound, hyperalgesia (aches and pains), fever
What is the secondary clock of the hypothalamus?
dorsomedial nucleus, is entrained by feeding schedules
What is proopiomelanocortin (POMC)?
neurons of the arcuate nucleus which respond to Leptin and Ghrelin from adipocytes and GI tract respectively; Leptin increases POMC activity and inhibits feeding and inhibits Neuropeptide Y and AGRP activity; Ghrelin promotes feeding by inhibiting POMC and activating NPY and AGRP
Is Ghrelin anorexogenic or orexogenic?
orexogenic; while Leptin is anorexogenic
What do the tuberomammillary nuclei produce?
histamine so that antihistamines which act on this nuclei affect the regulation of arousal and sleepiness
What is analgesia?
absence of pain in response to stimulation that would normally be painful
What is allodynia?
pain from a stimulus that does not normally provoke pain
What is hyperalgesia?
an increased response to a stimulus that is normally painful
What is neuralgia?
pain in distribution of nerve or nerves
What is a nocioceptor?
a receptor preferentially sensitive to a noxious stimulus or to a stimulus that would become noxious if prolonged, the stimuli differ in different tissues; they evoke autonomic reflexes and pain
What is parasthesia?
an abnormal sensation, whether spontaneous or provoked
What is pain?
an unpleasant sensory and emotional experience associated with actual or potential tissue damage; is always subjective
What factors contribute to pain?
duration, site/source, type
What is abnormal pain?
non-protective, chronic pain that can be peripheral or central
What are two types of nociceptive neurons?
Aδ fibers - thinly myelinated, fast pain, perception is well localized, specialized nerve endings, low or high threshold, conduct fast (10-40 m/s); C fibers - unmylenated, slow pain, perception poorly localized, free nerve endings, high threshold, conduct slowly (<2m/s)
Which rexed lamina do Aδ fibers synapse at? C fibers?
Aδ: I or V; C: II (substantia gelatinosa)
Where do pain fibers from the trigeminal nerve synapse?
caudalis nucleus of spinal tract of V; the secondary fiber then decussates and ascends with the contralateral spinothalamic tract
What system is part of the descending control of pain?
bulbospinal system, which regulates excitation and inhibits some of the peripheral signals of pain
What is the neospinothalamic tract?
from Aδ fibers, carries sharp, bright pain
What is the paleospinothalamic tract?
from C fibers, carries dull, aching pain
Where are opiod receptors located within the nocioceptive pathway?
limbic cortex, periaqueductal grey, spinal cord dorsal horn, trigeminal brainstem nuclear complex
What is capsaicin?
a chemical which activates the thermosensitive receptor vanilloid receptor 1 (TRPV1), causes release of substance P and CGRP, causes local destruction of nociceptive terminals, so it can be used to treat certain hyperalgesic conditions (herpes zoster)
What is neuropathic pain?
pain due to direct injury to the nervous system, burning, constant, throbbing, stabbing pain; can be mild/moderate/ or severe, associated with analgesia, hyperalgesia, allodynia; can be sympathetically mediated, non-sympathetically mediated, or central
What are conditions which produce neuropathic pain?
diabetic neuropathy, post herpetic neuralgia, cervical and lumbar radiculopathy, post thoracotom, post mastectomy, MS, phantom limb,
What effect does Substance P neurotransmitter have on nociception and what receptor does it act on?
Excitatory, NK-1
What effect does Glutamate neurotransmitter have on nociception and what receptor does it act on?
Excitatory, NMDA, AMPA, kainate, quisqualate
What effect does GABA neurotransmitter have on nociception and what receptor does it act on?
Inhibitory, GABAa, GABAb
What is the difference between nociception in adults and newborns?
Aβ fibers are much more excitatory in newborns and much more abundant such that touch may be receive as pain
What are the signs and symptoms of chronic pain?
immobility and wasting of muscle, depression of immune system, disturbed sleep, poor appetite, dependence on meds, alterations in moods
What are 7 pains you shouldn't ignore?
worst headache of your life, pain or discomfort in chest, throat, jaw, shoulder, arm or abdomen, pain in lower back or between shoulder blades, severe abdominal pain, calf pain, buring feet/legs, vague combined or medically unexplained pains
What is nocioception?
the neuronal response to tissue injury with or without an associated sensation
What can directly activate nociceptor nerve terminals?
mecahnically activated channels, ligand or H+ activated channels, tissue temp above 45 degree C and below 10,
What can indirectly activate nociceptor nerve terminals?
K+ from damaged cells, serotonin from platelets, histamine from activated mast cells, ATP from blood vessel endothelial cells, bradykinin produced by lysosomal enzymes acting on α2 globulins
What can cause sensitization or an increased response to a nocioceptive stimulus?
Arachidonic acid metabolites (prostaglandins and leukotrienes) by COX proteins, neuropeptides (substance P, calcitonin gene related peptide (CGRP), and neurokinin A)
What is the axon reflex?
the cause of the hyperalgesic response in tissue surrounding an initial nociceptive stimuli; caused by the action potentials stimulated by neuropeptides travels up axon to the branch point and spreads towards the soma and outward toward other axon branches and cause release of neuropeptides which stimulate mast cells, histamine release and edema
What are the two ascending pain systems?
lateral system (lateral STT, trigeminothalamic tract, has small receptive fields, fast CNS condunction, involved in discriminating location and intensity); medial system (spinoreticular, spinomesencephalic, dorsol columns, relay to intralaminar thalamic nuclei to anterior cingulate cortex, has large receptive fields, slow conduction, contain opiate receptors, cause affective responses
What causes referred pain?
visceral nociceptive afferent fibers that terminate on the same secondary neurons in the dorsal horn as somatic nociceptive afferent fibers
What is the pathway of visceral pain?
mediated largely by sympathetic nerves to spinal nerves
What is spinal pain gating?
modulation of nociceptive information transmited from dorsal horn to the brainstem by rubbing skin, massage because these actions activeate large and medium afferent fibers which activate inhibitory interneurons; acupuncture may follow the same mechanism
How do opiates activate the descending pain control pathway?
they inhibit interneurons which normally inhibit the PAG resulting in net excitation which send axons to the dorsal horn and inhibit dorsal horn neurons directly or via the activation of inhibitory interneurons
What is a neuroma?
a swirl of axons formed from regenerating peripheral nerves which are sensitive to mechanical stimuli
How does taking an aspirin help relieve pain?
aspirin inhibits the COX activity and decreases the discharge and rate of the nociceptive afferent fibers because fewer prostaglandins are formed