Unit 4

Specificity Theory

Pain as a separate sensory modality evoked by activity of specific receptors that transmit information to pain centers in forebrain

Pattern Theory

Pain receptors share endings or pathways with other sensory modalities; different patterns of activity of same neurons can be used to signal painful and non-painful stimuli

Gate Control Theory

Presence of neural gating mechanisms at segmental spinal cord level accounts for interaction between pain and other sensory modalities

Nauromatrix

Brain contains a widely distributed neural network, that contains somatosensory, limbic, and thalamocortical components that work together to create individual neural patterns

Neospinothalamic tract

rapid transmission of sensory information to thalamus; transmission of sharp-fast pain that is described as bright, sharp, or stabbing

Paleospinothalamic tract

slower transmission of sensory information to thalamus; responsible for dull, aching pain that is often accompanied by emotional responses.

Acute Pain

self-limiting pain that lasts less than 6 months

Chronic Pain

Persistent pain that lasts more than 6 months; lacks autonomic and somatic responses associated with acute pain; accompanied by debilitating responses

Pain threshold

pain at which stimulus is percieved as painful

Pain Tolerance

maximu intensity or duration of pain that a person is willing to endure before person wants an intervention for the pain

Nociceptive Pain

Nociceptors (pain receptors) activated in response to actual or impending tissure injury

Neuropathic Pain

Arises from direct injury to nerves

Cutaneous Pain

Sharp, burning pain that originates in skin or subcutaneous tissues

Deep Somatic Pain

More diffuse and throbbing pain that originates in body structures

Visceral Pain

Diffuse and poorly defined pain the originates in an organ and results from stretching, distention, or ischemia of tissues

Referred Pain

Pain that originates at a visceral site and is perceived as originating in part of the body wall normally innervated by neurons entering same segment of nervous system

Allodynia

pain due to non-injury skin stimulus

Hyperalgesia

extreme sensitivity to pain

Paresthesias

nerve (or neuropathi) pain sensation; i.e. numbness and tingling, pins and needles

Analgesia

relief from pain

Phantom Limb Pain

pain that follows amputating of a limp(partial or complete) that begins as sensations of tingling, heat and cold, or heaviness followed by burning, cramping, or pain

Migraine without Aura

pulsatile, throbbing, unilateral headache that typically lasts 1 to 2 days and aggravated by routine physical activity

• N/V

• Photosensitivity

• Phonosensitivity

• Visual disturbances are common including hallucinations

• Prodromal symptoms precede attack by hours or days

Migrane with Aura

has reversible visula symptoms, fully reversible sensory symptoms, and fully reversible speech disturbances or neurologic symptoms that precede the headache.

Aura

uncommon sensation that develops over 5 to 20 minuets and can last up to an hour

Cluster Headache

occur in cluster over weeks or months with severe, unrelenting unilateral pain, followed my remission period; More frquent in men and women and typically begin in their 30’s

Cluster Headache Clinical Manifestations

• Rapid onset and peaks in approx. 10 to 15 minuets

• Last 15 to 180 minuets

• Pain behind eye radiates to ipsilateral trigeminal nerve

• Restlessness

• Conjunctival redness

• Lacrimation on one side

• Nasal congestion

• Rhinorrhea

• Forehead and facial swelling

• Miosis, ptosis, and eyelid edema

Tension-Type Headache

Most common type of headache; usually not sufficiently severe that it interferes with daily activities

Tension-Type Headache Clinical Manifestations

• Dull, aching, diffuse, nondescript headaches, occurring in a hatband distribution around the head

• Not associated with nausea or vomiting or worsened by activity

Asparin and other nonsteroidal anti-inflammatory drugs (NSAIDs)

Effective in controlling pain because they block the enzymes needed for prostaglandin synthesis

Nonpharmacologic treatment of migranes

Avoidance of triggers, such as foods or smells that precipitate an attack

Hyperthermia

Increased body temperature above the normal

Malignant hyperthermia

Autosomal dominant metabolic disorder where heat is generated by uncontrolled skeletal muscle contraction producing severe and potential fatal manifestation; During anesthesia skeletal muscle will go rigid

Neuroleptic Malignant Syndrome

a severe reaction to neuroleptic medications

Neuroleptic Malignant Syndrome Clinical Manifestations

• Explosive onset

• Hyperthermia, muscle rigidity, altered consciousness, and autonomic nervous system dysfunction

• Tachycardia, cardiac dysrhythmias, labile blood pressure, dyspnea, & tachypnea

Muscular Atrophy

Normally innervated muscle is not used for long periods leading muscle cell shrinkage, they lose much of their contractile protein, and weaken

Muscular Dystrophy

A genetic disorder that produces progressive deterioration of skeletal muscles due to mixed muscle cell hypertrophy, atrophy, and necrosis

Myasthenia Gravis

Disorder of neuromuscular junction transmission affecting communication between motoneuron and innervated muscle cell

Myasthenia Gravis Cause

Autoimmune disease caused by anitbody-mediated loss of acetylcholine receptors in the neuromuscular junction

Myasthenia Gravis Clinical Manifestations

• Weakness & fatigue with sustained effort

• Initial symptoms - eye and periorbital muscles (commonly affected) with ptosis due to eyelid weakness or diplopia due to extracellular muscle weakness

• Chewing & swallowing difficulties

• Extremity weakness - climbing stairs & lifting objects are difficult

• With disease progression, lower face muscles impacted - causing speech impairment

• Commonly, symptoms are least evident in morning and worsen with effort as the day progresses

Myasthenic Crisis

sudden exacerbation of muscle weakness leading to respiratory failure and requiring emergency treatment such as ventilatory support and airway protection

Peripheral Neuropathy

any primary disorder of the peripheral nerves

Peripheral Neuropathy Results

muscle weakness, with or without atrophy and sensory changes

Mononeuropathy

single nerve involvement

Polyneuropathy

involves demyelination of axonal degeneration of multiple peripheral nerves leading to symmetric sensory, motor, or mixed sensorimotor deficits; typically, longest axons involvement first and symptoms begin in distal extremities

Guillain-Barre Syndrome

acute immune-mediated polyneuropathy

Guillain-Barre Syndrome Clinical Manifestations

• Progressive ascending muscle weakness of limbs, producing a symmetric flaccid paralysis

• Paresthesia & numbness

• Ventilator is required if paralysis involves respiratory muscles

• Autonomic nervous system involvement causes postural hypotension, arrhythmias, facial flushing, abnormalities of sweating, & urinary retention

• Pain

Parkinson’s Disease

Degenerative disorder of basal ganglia function with progressive destruction of nigrostriatal leading to a decrease/deficiency in dopamine.

Parkinson’s Disease Clinical Manifestations

• Tremor

• Pill-rolling hand/fever movement

• Nuchal Rigidity

• Bradykinesia

Amyotrophic Lateral Sclerosis (ALS)

Devastating neurologic disorder that selectively affects motor function and destroys motor neurons

Manifestations of UMN in ALS

lesions include weakness, spasticity or stiffness, and impaired fine motor control

Manifestations of LMN

lesions include fasciculations, weakness, muscle atrophy, and hyporeflexia

Early symptom of ALS

muscle cramps involving distal legs

Common clinical manifestations of ALS

slow progressive weakness and atrophy in distal muscles of one upper extremity followed by regional spread of clinical weakness

Mean survival period for patients with ALS

2 to 5 years from onset of symptoms

Multiple Sclerosis(MS)

inflammation and destruction of Central Nervous System(CNS) myelin resulting in plaque buildup in the brain

Relapsing-remitting

characterized by episodes of acute worsening with recovery and a stable between relapses

Seconday progressive

gradual neurologic deterioration with or without superimposed acute relapses in a person with previous relapsing-remitting disease

Primary progressive

nearly continuous neurologic deterioration from onset of symptoms

Progressive relapsing

gradual neurologic deterioration from the onset of symptoms but with subsequent suptimposed relapses

Spinal Cord Injury(SCI)

Damage to spinal cord neural element caused my motor vehicle collisions, falls, violence, and sporting activities

Central Cord Syndrome

injury predominantly in central gray or white matter of the cord

Anterior Cord Syndrome

caused by damage from infarction of anterior spinal artery, resulting in damage to the anterior two thirds of the cord

Multiple Sclerosis (MS)

• healthy person common acute paresthesia’s, optic neuritis, diplopia, or specific types of gaze paralysis

• Paresthesias’s, spasticity pain

• Abnormal gait, bladder and sexual dysfunction, vertigo, nystagmus, fatigue, and speech disturbance ususally last days to weeks and completely or partially resolve

• Psychological manifestations (mood swings)

• Depression, euphoria, inattentiveness, apathy, forgetfulness, and loss of memory

• Fatigue (common)

SCI involvement

• damage to the vertebral column, supporting ligaments, and spinal cord

• Commonly involves both sensory and motor function

• Complete & Incomplete

Brown-Sequard Syndrome

results from damage to hemisection of anterior and posterior cord

• ipsilateral loss of voluntary motor function from corticospinal tract

• Proprioception loss with contralateral loss of pain and temperature sensation from. lateral spinothalamic tracts for all levels below lesion

Cauda Equina Syndrome

damage to lumbosacral nerve roots in spinal canal results in LMN & sensory neuron damage

• Functional deficits present as patterns of asymmetric flaccid paralysis, sensory impairment, & severe asymmetric pain

• Emergent surgery is indicated

Simple or Linear

Break in the continuity of bone

Comminuted

Splintered or multiple fractures lines

Depressed

Bone fragments embedded into brain tissue

Basilar

Fracture of bones that form the base of the skull

Full Conciousness

• Awake, alert, and oriented to time, place, and person

• Comprehends spoken and written word

• Able to express ideas

Confusion

• Disoriented to time, place, or person

• Memory difficulty

• Difficulty following commands

Lethargy

• Oriented to time, place, and person

• Very slow in mental processes, motor activity, and speech

• Responds to pain appropriately

Obtundation

• Responds verbally with a word

• Arousable with stimulation

• Responds appropriately to painful stimuli

• Follows simple commands

• Appears very drowsy

Stupor

• Unresponsive except to vigorous and repeated stimuli

• Responds appropriately to painful stimuli

• Lies quiet with minimal spontaneous movement

• May have incomprehensible sounds and/or eye openning

Coma

• Does not respond appropriately to stimuli

• Sleeplike state with eyes closed

• Does not make any verbal sounds

Signs of Decreased LOC Earliest Signs

Altered mental status i.e. inattention, mild confusion, disorientation, and blunted reponsiveness

Hypoxia

a deprevation of oxygen with maintained blood flow

Ischemia

Reduced or interrupted blood flow

Focal cerebral ischemia

Stroke

Global cerebral ischemia

Myocardial infarction

Intracranial Pressure (IPC)

common mechanism for brain injury when increased; can obstruct cerebral blood flow, destroy brain cells, displace brain tissue, and damage delicate brain structures

Normal ICP

0 to 15 mmHg

Monroe-Kellie Doctrine

dynamic equilibrium between cranial cavity contents including 80% brain tissue, 10% blood, and 10% cerebrospinal fluid(CSF)

Uncal

involved cerebral peduncle, oculomotor nerve, posterior cerebral artery, cerebellar tonsil, respiratory center

Uncal Clinical manifestations

• Hemiparesis

• Pupil dilation

• Visual field loss

• Respiratory arrest

Hydrocephalus

Abnormal increase in CSF volume in the ventricular system of the brian; Enlargement of CSF compartment occurs

Communicating

Decreased absorption of CSF

Noncommunicating

Overproduction of CSF

Coup-Contrecoup Injury

Blunt force to the head accelerates brain within skull brain decelerates abruptly hitting inner skull surfaces

Coup

direct contusion of brain at site of external force

Contrecoup

rebound injury on the opposite side of brain

Concussion

an immediate and transient loss of consciousness accompanied by a brief period of amnesia after a blow to the head

Postconcussion syndrome Clinical manifestations

• Headache

• Irritability

• Insomnia

• Poor concentration and memory

Epidural Hematoma

Positive Level of Consciousness followed by lucid interval and subsequent Level of Consciousness decline

Subdural Hematoma

tear in small bridging veins that connect veins on cortex surface to dural sinuses

Subdural space

area where hematoma develops between the dural and arachnoid space

Traumatic Intracerebral Hematomas

may be single or mutiple, occur in any brain lobe, most common in frontal or temporal lobes

Ischemic Strokes

interruption of blood flow in a cerebral vessel (i.e. a blood clot); most common type of strokes 70% to 80% of all strokes

Hemorrhagic Strokes

bleeding into brain tissue from a blood vessel rupture (i.e. hemorrhage or ruptured blood vessel); secondary to hypertension, aneurysms, arteriovenous malformations, head injury, or blood dycrasias