Study guide Essay
1.Review the anatomy of the brain. Which portion is responsible for keeping you awake, controlling thought, speech, emotions and behavior, maintaining balance and posture? Emotions and behavior are controlled by the hypothalamus (p.455) The cerebellum is responsible for maintaining balance and posture (p.455) The reticular formation is essential for maintaining wakefulness and in conjunction with the cerebral cortex is referred to as the reticular activating system (p.450) The Broca speech area is rostral to the inferior edge of the premotor area on the inferior frontal gyrus. It is usually on the left hemisphere and is responsible for the motor aspects of speech. Damage to this area leads to expressive aphasia or dysphasia (p.452) The Wernicke area is responsible for reception and interpretation of speech, and dysfunction may result in receptive aphasia or dysphasia (p.452) The prefrontal area of the frontal lobe is responsible for goal-oriented behavior, short-term or recall memory, and the elaboration of thought and inhibition on the limbic areas of the CNS. (p.452)
2. Know the function of the arachnoid villi.
The arachnoid villi function as one-way valves directing CSF outflow into the blood but preventing blood flow into the subarachnoid space (p.461)
3. Where is the primary defect in Parkinsons disease and Huntingtons? The inferior-most portion of the basal ganglia is the substantia nigra, which synthesizes dopamine, a neurotransmitter and precursor of norepinephrine. Its dysfunction is associated with Parkinsons disease (p.455) The basal ganglia system is believed to exert a fine-tunning effect on motor movements. Parkinsons disease and Huntingtons diseare are conditions associate with defects of the basal ganglia. (p.452)
4. What is the function of the CSF? Where is it produced? Where is it absorbed? The function of the CSF is to protect the intracranial and spinal cord structures from jolts and blows (p. 461). It also prevents the brain from tugging on meninges, nerve roots, and blood vessels (p.461). The choroid plexuses in the lateral, third, and fourth ventricles produce the major portion of CSF. (p.461) The CSF does not accumulate. It is reabsorbed into the venous circulation through the arachnoid villi (p.461).
5. Review blood flow to the brain. p. 462 – The internal carotid arteries (supply greater amount of blood flow) take their origin from the common carotid arteries, enter the cranium thru the base of the skull, and pass thru the cavernous sinus, They then divide into the anterior and middle cerebral arteries. The vertebral arteries, posteriorly, originate as branches off the subclavian arteries, pass thru the transverse foramina of the cervical vertebrae, and enter the cranium thru the foramen magnum. They join at the junction of the pons and medulla oblongata to form the basilar artery. The basilar artery divides at the level of the midbrain to form paired posterior cerebral arteries. Three major paired arteries perfuse the cerebellum and brainstem and originate from the posterior arterial supply; the posterior inferior cerbellar artery, off the vertebral artery; and the anterior inferior cerebellar and superior cerebellar ateries, off the basilar artery. The basilar artery also gives rise to small pontine arteries. The large arteries on the surface of the brain and their branches are called superficial arteries (conducting arteries). The small branches that project into the brain are termed projecting arteries (nutrient arteries)
6. What is the gate control theory of pain?
According to this theory, pain transmission is modulated by a balance of impulses transmitted to the spinal cord by large A-delta and small C fibers. These fibers terminate on inhibitory interneurons in the substantia gelatinosa (laminae in the dorsal horn of the spinal cord). Cells in the substantia gelatinosa function as a gate, regulating transmission of impulses to the CNS. Stimulation of non-nociceptive larger A fibers such as touch, vibration or thermal stimuli, cause the cells in the substantia gelatinosa to “close the pain gate” which diminishes pain perception. Small fiber input inhibits cells in the substantia gelatinosa and “ opens the pain gate” enhancing pain perception. The CNS, through efferent pathways, may also close, partially close, or open the gate. (p.482)
7. Know the type of nerve fibers that transmit pain impulses. Medium sized A delta fibers are stimulated by mechanical deformation (mechanonociceptors) and/or extremes of temperature(mechanothermal nociceptors) Occurs quickly. Carry well localized, sharp pain sensations and are important in initiating rapid reactions to stimuli (fast pain). Mechanical, thermal, and chemiacal nociception are transmitted by excitation of polymodal nociceptors and are carried on small unmyelinated C fibers. The small unmyelinated C polymodal nociceptors are responsible for the transmission of the diffuse burning or aching sensations that follow (slow pain). (p.483) Table 15.1
Location of ReceptorProvoking Stimuli
SkinPricking, cutting, crushing, burning, freezing
GI tractEngorged or inflamed mucosa, distention or spasm of smooth muscle, traction on mesenteric attachment Skeletal muscleIschemia, injuries of connective tissue sheaths, necrosis, hemorrhage, prolonged contraction, injection of irritating solutions BonePeriosteal injury, inflammation, fractures, tumors
JointsSynovial membrane inflammation
HeadTraction, inflammation, or displacement of arteries, meningeal structures, and sinuses; prolonged muscle contraction HeartIschemia and inflammation
8.Where in the CNS does pain perception occur?
p.483 The cell bodies of primary-order neurons or pain-transmitting neurons reside in the dorsal root ganglia just lateral to the spine along the sensory pathways that penetrate the posterior part of the cord. The second order neurons are found in the dorsal horn (p.484) Most nociceptive information tranvels by means of ascending columns in the lateral spinothalamic tract (also called the anterolateral funiculus). The principal target for nociceptive afferents is the thalamus (the major relay station of sensory information in general) Third order neurons project to portions of the CNS involved in the processing and interpretation of pain, the chief areas being the reticular and limbic systems and cerebral cortex. (p 484)
9. Know different clinical descriptions of pain; pain threshold/tolerance
The most widely used clinical classifications for pain are based on the inferred neurophysiologic mechanisms, temporal aspects, etiology, and region affected. Usually described as nociceptive or non-nociceptive, and by duration, either acute or chronic. acute pain-a protective mechanism that alerts the individual to a condition or experiece that is immediately harmful to the ody and mobilizes the individual to take prompt action to relieve it; transient, usually lasting seconds to days; begins suddenly and relieved after the chemical mediators that stimulate pain receptors are removed. Acute pain arises from cutaneous and deep somatic tissue, or from visceral organs and can be classified as acute somatic, acute visceral, and referred. somatic- superficial, arising from connective tissue, muscle or bone, and skin. It is either sharp and well localized or dull, aching, throbbing, and poorly localized as seen in polymodal C fiber transmission. visceral pain- refers to pain in internal organs and the lining of body cavities with an aching, gnawing, throbbing, or intermittent cramping quality. It is transmitted by sympathetic afferents and is poorly localized because of the lesser number of nociceptors in the visceral structures. referred pain- pain that is felt in an area removed or distant from its point of origin.
Impulses from many cutaneous and visceral neurons converge on the same ascending neuron, and the brain cannot distinguish between the two. chronic pain- usually defined as lasting at least 3 months and well beyond the expected healing time following the initial onset of tissue damage or injury. Neuroimaging studies have demonstrated brain changes in those with chronic pain that may lead to cognitive deficits and decreased ability to cope with pain. cancer pain- often chronic and associated with neuropathies. neuropathic pain- results from primary injury to the peripheral or central nervous system and is not the result of pain signaling from peripheral tissues or organs
peripheral neuropathic pain- caused by peripheral nerve trauma, diabetic or alcohol abuse-induced neuropathy, carcinoma, nutritional deficiencies, and HIV. central neuropathic pain- caused by a lesion or dysfunction in the CNS hemiagnosia pain- form of central pain associated with stroke that produces paralysis and hypersensitivity/allodynia on one half of the body phantom limb pain- pain that an individual feels in an amputated limb after the stump has completely healed. pain threshold- the point at which a stimulus is perceived as pain and it does not vary significantly among people or in the same person over time.
Pain tolerance- the duration of time or the intensity of pain that an individual will endure before initiating overt pain response and is generally decreased with repeated exposure to pain. It is influenced by the person’s cultural perceptions, expectations, role behaviors, physical and mental health, gender, fatigue, anger, boredom, apprehension, and sleep deprivation. Tolerance may be increased by alcohol consumption, persistent use of pain medication, hypnosis, warmth, distracting activities, and strong beliefs or faith. (p. 490-491, 6th ed)
10. Know endogenous opioids.
Endogenous opiods are a family of morphine-like neuropeptides that inhibit transmission of pain impulses in the spinal cord, brain, and periphery. Their receptors also play a role in various CNS, GI, immune, and other organ system disorders. They also modulate stress and anxiety, feeding behavior, cough suppression, immune and inflammatory responses, and alcohol intake. There are three distinct types of opioid receptors found in the body: mu, kappa, and delta. There are 4 types of opioid neuropeptides: 1.) enkephalins, 2.) endorphins, 3.) dynorphins, and 4.) endomorphins enkephalins: There are 2 types: Met-enkephalin and Leu-enkephalin and their ratio is 4:1, respectively. They are foud concentrated in the hypothalamus, the PAG matter, the nucleus raphe magnus of the medulla, and the dorsal horns of the spinal cord.
Endorphins: The synthesis and activity of B-endorphin are concentrated in the hypothalamus and the pituitary gland. It is purported to produce a greater
sense of exhiliration than all of the other endorphin types. dynorphins: are the most potent of the endogenous neurohormones and are found in the hypothalamus, the brainstem, the PAG-RVM system, and the spinal cord. They bind strongly to kappa receptors and serve to impede pain signals, but can incite pain through mechanisms of up-regulation. endomorphins: have potent analgesic, GI, and anti-inflammatory effects. They show the highest affinity and selectivity for mu-receptors. (p. 488-490, 6th ed)
11. What are the two types of fibers that transmit the nerve action potentials generated by excitation of any of the nociceptors.
The nerve action potentials generated by excitation of any of these nociceptors travel along these two fiber types to reach the spinal cord. Nociceptive transmission occurs more quickly in Aδ fibers than it does through C fibers. (1) Aδ fibers carry well localized, sharp pain sensations and are important ininitiating rapid reactions to stimuli (fast pain). The small (2) unmyelinated C polymodal nociceptors are responsible for the transmission of the diffuse burning or aching sensation that follow (slow pain). (p. 483, 6th ed)
12. What is the relationship between epinephrine and body temperature? Epinephrine causes vasoconstriction, stimulates glycolysis, and increases metabolic rates, thus increasing heat production. Epinephrine and norepinephrine produce a rapid, transient increase in heat production by raising the body’s basal metabolic rate in Chemical thermogenesis (p. 496, 6th ed) Endogenous pyrogens are produced by phagocytic cells as they destroy microorganisms within the host. The endogenous pyrogens act on the preoptic nucleus of the hypothalamus. Centers in the hypothalamus and brainstem signal an increase in heat production and heat conservation to raise body temperature to the new set point. Peripheral vasoconstriction occurs with shunting of blood from the skin to the body core. Epinephrine release increases metabolic rate, and muscle tone increase. Decreased release of vasopressin reduces the volume of body fluid to be heated. Shivering may occur. Body temperature is maintained at the new level until the fever breaks. (p. 496-497, 6th ed).
13. Know mechanisms of heat production and heat loss.
Mechanisms of Heat Production:
1.)Chemical Reactions of Metabolism: these processes occur in the body core (primarily the liver) and are in part responsible for the maintenance of core temperature
2.) Skeletal Muscle Contraction: Skeletal muscles produce heat through two mechanisms: gradual increase in muscle tone and production of rapid muscle oscillations-shivering
3.) Chemical Thermogenesis: results from the release of epinephrine and norepinephrine that produce a rapid, transient increase in heat production by raising the body’s BMR. Produces a quick, brief rise in BMR, whereas hormone thyroine triggers a slow, prolonged rise. Occurs in brown adipose tissue that is rich with mitochondria and blood vessels and is essential for nonshivering thermogenesis. Mechanisms of Heat Loss:
1.) radiation: refers to heat loss through electromagnetic waves. If the temperature of the skin is greater than the temp of the air, the skin will lose heat to the air.
2.) conduction: regers to heat loss by direct molecule-to-molecule transger from one surface to another. The warmer surface loses heat to the cooler surface.
3.) convection: the transfer of heat through currents of gases or liquids. 4.) vasodilation: diverts core-warmed blood to the surface of the body 5.) decreased muscle tone: to decrease heat production, muscle tone may be moderately reduced and voluntary muscle activity curtailed
6.) evaporation: evaporation of body water from the surface of the skin and the linigs f the mucous membranes is a major source of heat reduction
7.) increased pulmonary ventilation: exchaning air with the environment through thte normal pulmonary ventilation provides some heat loss, although it is minimal
8.) voluntary mechanisms: response to high body temps, people physically stretch out 9.) adaptation to warmer climates: the body of an individual who moves from a cooler to a warmer climate undergoes a period of adjustment
(p. 496-497, 6th ed)
14.Know heat exhaustion and heat stroke?
Heat Exhaustion: the result of prlonged high core or environmental temperatures. Causes the hypothalamic response of profound vasodilation and profuse sweating. After a prolonged period, the hypothalamic responses produce dehydration, decreased plasma volumes, hypotension, decreased cardiac output, and tachycardia. Feel dizzy, weak, and nauseated. Ceasing activity decreases muscle work causing decreased heat production. Lying down redistributes vascular volume. The individual should be encouraged to drink warm fluids to replace fluid lost through sweating. Heat Stroke:potentially lethal consequence of a breakdown in control of an overstressed thermoregulatory center. Brain cannot tolerate temps over 104.9. The regulatory center may cease to function appropriately. Results in irritability, stupor, confusion, or coma. High core temps and vascular collapse produce cerebral edema, degeneration of the CNS, and renal tubular necrosis. Treatment: removing the person from the warm environment and cooling with cooling blanket or cool water bath. Too rapid surface cooling may cause peripheral vasoconstriction preventing core cooling. Children are more susceptible because they produce more metabolic heat when exercising, have a greater surface area:mass ratio, and their sweating capacity is less than adults. (p. 500, 7th ed)
15.Define the different stages of sleep.
Normal sleep has two phases that can be documented by EEG: REM and non-REM, or slow wave sleep. NREM sleep is divided into 3 stages, based on changes in EEG patterns: 1.) awake: wakefulness with eyes closed and predominated by alpha waves (8-25 Hz) 2.) light sleep: (N1) with alpha waves (6-8 Hz) interspersed with low frequency theta waves; slow eye movements (3-8% of sleep time)
3.) N2: further slowing of the EEG (4-7 Hz) with the presence of sleep spindles and slow eye movements (45-55% of sleep time)
4.) N3: low frequency (1-3 Hz) high amplitude delta waves with occasional sleep spindles; no eye movements (15-20% of sleep time)
REM sleep: time of most dreaming (20-25% of sleep time); occurs for 5-60 minutes about every 90 minutes beginning after 1-2 hours of NREM sleep; characterized by conjugate rapid eye movement in all directions. REM sleep is controlled by the pontine reticular formation. (p. 502 & 503, 7th ed)
16. Discuss disorders of the conjunctiva of the eye.
Conjunctivitis may be caused by bacteria, viruses, allergies, or chemical irritations. The inflammatory response produces redness, edema, pain, and lacrimation. Treatment is related to cause. Acute bacterial conjunctivitis (pinkeye): highly contagious and often is caused by gram-positive organisms (Staphylococcus, Haemophilus, Proteus), although other bacteria may be involved. The onset is acute, characterized by mucopurulent drainage from one or both eyes. The disease often is self-limiting and resolves spontaneously in 10 to 14 days. Antibiotic eyedrops usually are effective.
Viral conjunctivitis: caused by an adenovirus. Symptoms vary from mild to severe. Some strains of virus cause conjunctivitis and pharyngitis (pharyngoconjunctival fever), and others cause keratoconjunctivitis. Both diseases are contagious, with watering, redness, and photophobia. Treatment is symptomatic. Allergic conjunctivitis: associated with a variety of antigens, including pollens. Ocular itching is associated with photophobia, burning, and gritty sensations in the eye. Treatment is symptomatic and may include antihistamines, steroids, and vasoconstrictors.
Chronic conjunctivitis: is the result of any persistent conjunctivitis. The cause requires identification for effective treatment. Trachoma (chlamydial conjunctivitis): is caused by Chlamydia trachomatis. It often is associated with poor hygiene and is the leading cause of preventable blindness in the world. The severity of the disease varies, but it can involve inflammation with scarring of the conjunctiva and eyelids causing distorted lashes to abrade the cornea leading to corneal scarring and blindness. Chlamydial organisms are sensitive to local or systemic antibiotics. (p. 506 & 507, 6th ed)
17. Which part of the eye controls movement of the eye?
Cranial nerves III (oculomotor), IV (trochlear), VI (abducens). Six extrinsic eye muscles allow gross movements and permit the eyes to follow a moving object: Inferior oblique, superior oblique, lateral rectus, medial rectus, superior rectus, and levator palpebrae superioris (pg 528)
18. What part of the brain must be functioning for cognitive operations? Reticular activating system regulates aspects of attention and information processing and maintains consciousness. Cognitive cerebral functions require a functioning reticular activating system. (pg 528). The Cerebrum controls all voluntary actions in the body.
19. Discuss the types of mid-brain dysfunction and its physical symptoms. Midbrain (mesencephalon) dysfunction: roving eye movements cease and the eyes become immobile and directed ahead. Eyes may turn down and inward. Oculovestibular reflexes become inconsistent and abnormal. Loss of Bell phenomenon (upward deviation of eyes on stimulation). (pg 531 table 17-5). The inferior-most portion of the basal ganglia is the substantia nigra, which synthesizes dopamine, a neurotransmitter and precursor of norepinephrine. Its dysfunction is associated with Parkinson’s disease and drug addiction. The cerebral aqueduct (aqueduct of Sylvius), which carries CSF, traverses the tracts of third and fourth cranial nerves. The obstruction of this aqueduct is often the cause of hydrocephalus (pg 459)
20. Know the best prognostic indicator of recovery of consciousness and functional outcome after a brain event. An isoelectric, or flat, electroencephalogram (EEG) for a period of 6-12 hours in a person who is not hypothermic and has not ingested depressant drugs indicates that no mental recovery is possible=brain is already dead. (pg 533)
21. Know vomiting with which CNS injuries.
Vomiting often accompanies CNS injuries that involve the vestibular nuclei or its immediate projections, particularly when double vision is present, impinge directly on the floor of the 4th ventricle; or produce brainstem compression secondary to increased intracranial pressure (pg 533)
22. Define seizure and status epilepticus. What is the medical significance? Know benign febrile seizures. Seizure is a sudden, transient disruption in brain electrical function caused by abnormal excessive hypersynchronous discharges of cortical neurons. Etiologic factors in seizures include: cerebral lesions, biochemical disorders, cerebral trauma, and epilepsy. Conditions that may produce a seizure are metabolic defects, congenital malformations, genetic predisposition, perinatal injury, postnatal trauma, myoclonic syndromes, infection, brain tumor, and vascular disease. Seizures may be precipitated by hypoglycemia, fatigue, emotional or physical stress, fever, large amounts of water ingestion/hyponatremia, constipation, use of stimulant drugs, withdrawal from depressant drugs or alcohol, hyperventilation/respiratory alkalosis, and some environmental stimuli such as blinking lights, a poorly adjusted tv screen, loud noises, certain odors, or being startled. Immediately before or during menses women may have increased seizure activity (pg 550) Status epilepticus in adults is a state of continuous seizures lasting more than 5 min, or rapidly recurring seizures before the person has fully regained consciousness lasting more than 30 min. Can arise from abnormal persistence of excessive excitation or ineffective recruitment inhibition.
The person is still in a postictal state (state that follows an epileptic seizure and returns to baseline) when the next seizure begins. Most often results from abrupt discontinuation of antiseizure meds but also may occur in untreated or inadequately treated persons with seizure disorders. The situation is a medical emergency because of the resulting cerebral hypoxia. Mental retardation, dementia, and other brain damage and even death are serious threats. Aspiration is also a great risk. (pg 553) Simple febrile seizures occur in 2-5% of children. They are benign. Pathogenesis is unknown. A familial incidence of simple febrile seizures indicates a genetic predisposition to the problem. Factors that contribute to susceptibility include age, degree, and rate of temperature elevation, and nature of the particular fever-inducing illness. Any disorder producing a high fever may provoke benign febrile seizures in susceptible children. (pg 679)
23. Know the characteristics of closed head injury.
Closed (blunt trauma) involves either the head striking a hard surface or a rapidly moving object striking the head. The dura mater remains in tact, and brain tissues are not exposed to the environment. Most closed/blunt trauma is mild and causes mild concussion and classic cerebral concussion. (pg 582) Mild concussion (mild traumatic brain injury) is characterized by immediate but transitory clinical manifestations. CSF pressure rises, and ECG and EEG changes occur without a loss of consciousness. The glascow coma scale is 13-15. The initial confusional state lasts from 1-several minutes, possible with amnesia for events preceding the trauma (retrograde amnesia) Anterograde amnesia also may exist transiently. Persons may experience head pain and complain of nervousness and “not being themselves” for up to a few days. (pg 587). Classic Cerebral Concussion is any loss of consciousness (can last up to 6 hours) accompanied by retrograde and anterograde amnesia. Transient cessation of respiration can occur with brief periods of bradycardia, and a decrease in blood pressure lasting 30 seconds or less. Vitals stabilize within seconds to within normal limits. This is a phenomenon of physiologic, neurologic dysfunction without substantial anatomic disruption. A confusional state exists for hours to days. The individual experiences head pain, nausea, and fatigue. Attentional and memory system impairments may persist for weeks to months and may include inability to concentrate and forgetfulness. Mood and affect changes may persist for weeks to months and may include nervousness, anxiety reactions, depression, irritability, fatigability, and insomnia. (pg 588)
24. Define dyskinesia. Types? Characteristics?
Dyskinesia is an unnatural movement (pg 561).
Tardive dyskinesia is a side effect of conventional antipsychotics that develops in 15-20% of schizophrenics after several years of treatment. This condition is characterized by tic-like jerky movements, such as smacking the lips or flicking the tongue, unsteady gait, or rocking back and forth when seated, sedation, hypotension, akathisia (motor restlessness), constipation, weight gain, amenorrhea, hepatoxicity (less common) and electrocardiographic changes. (pg 646). Tardive dyskinesia is the involuntary movement of the face, trunk, and extremities. Occurs in individuals with Parkinson’s disease and those who take first or second generation antipsychotic drugs. The drugs cause denervation hypersensitivity, thereby mimicking the effect of excessive dopamine. Most common symptom is rapid, repetitive, stereotypic movements. The most characteristic movements of tardive dyskinesia include continual chewing with intermittent protrusions of the tongue, lip smacking, and facial grimacing. Paroxysmal dyskinesias are abnormal, involuntary movements that occur as spasms. (pg 562)
25. Know the stages of intracranial hypertension.
Stage 1: vasoconstriction and external compression of the venous system occur in an attempt to further decrease the ICP. Thus, ICP may not change because of the effective compensatory mechanisms and there may be few symptoms. Small increases in volume, however, cause an increase in pressure, and the pressure may take longer to return to baseline. Detected with ICP monitoring Stage 2: Continued expansion of intracranial contents. The resulting increase in IC may exceed the brain’s compensatory capacity to adjust. The pressure begins to compromise neuronal oxygenation, and systemic arterial vasoconstriction occurs in an attempt to elevate the systemic blood pressure sufficiently to overcome the IICP. Clinical manifestations at this stage are subtly and transient, including episodes of confusion, restlessness, drowsiness, and slight pupillary and breathing changes. Stage 3: ICP begins to approach arterial pressure, the brain tissues begin to experience hypoxia and hypercapnia, and the individual’s condition rapidly deteriorates. Clinical manifestations include decreasing levels of arousal or central neurogenic hyperventilation, widened pulse pressure, bradycardia, and pupils become small and sluggish Stage 4: brain tissue shifts (herniates) from the compartment of greater pressure to a compartment of lesser pressure and IICP in one compartment of the cranial vault is not evenly distributed throughout the other vault compartments. With this shift in brain tissue, the herniating brain tissue’s blood supply is compromised, causing further ischemia and hypoxia in the herniating tissues. The volume of content within the lower pressure compartment increases, exerting pressure on the brain tissue that normally occupies that compartment, and impairing blood supply. Small hemorrhages often develop in the involved brain tissue. Obstructive hydrocephalus may occur. The herniation process markedly and rapidly increases ICP. Mean systolic arterial pressure soon equals ICP and cerebral blood flow ceases at this point. (pg 556-557)
26. Know normal intracranial pressure. How does body compensate for increased ICP? Pg. 557. Normal intracranial pressure is 5 to 15 mmHg, or 60 to 180 cm H2O. A rise in intracranial pressure necessitates an equal reduction in volume of the other contents. The most readily displaced content of the cranial vault is CSF. If intracranial pressure remains high after CSF displacement out of the cranial vault, cerebral blood volume is altered; this causes stage 1 intracranial hypertension. Vasoconstriction and external compression of the venous system occur in an attempt to further decrease the intracranial pressure
27. Know the most critical index of nervous system dysfunction/function. Pg. 529. Level of consciousness is the most critical clinical index of nervous system function or dysfunction. An alteration in consciousness indicates either improvement or deterioration of the individual’s condition.
28. What is responsible for the tremors associated with Parkinsons Disease? Pg. 573. Parkinsonial tremor appears to result from instability of feedback from the basal ganglia to the cerebral cortex caused by loss of the inhibitory influence of dopamine in the basal ganglia. Increased oscillation in the normal feedback cycles of the motor outflow feedback circuit when the muscles are at rest produces the tremor.
29. Define concussion. Know the different grades of concussion. Pg. 590.
Mild concussion involves temporary axonal disturbances. Consciousness is not lost 1). Grade 1 confusion and disorientation accompanied by amnesia (momentary) 2). Grade 2 momentary confusion and retrograde amnesia that develops 5-10 minutes after injury 3). Grade 3 confusion and retrograde amnesia present from the time of impact and persists for several minutes. Cerebral concussion (grade 4) involves diffuse cerebral disconnection from the brainstem reticular activating system and in a phenomenon of physiologic and neurological disfunction without substantial autonomic disruption. Loss of consciousness can last to 6 hours and reflexes are lost. A confusional state may persist for hours to days. The individual may complain of nausea, head pain, and fatigue. An initial decrease in BP, HR, and cessation of respirations occurs with normalization of vital signs within a few seconds. Nervousness, anxiety, depression, irritability, fatigue, and insomnia may persist for weeks to months.
30. Know coupe and countercoup brain injuries and how they happen. Pg. 585. Contusion and bleeding occur because of small tears in blood vessels resulting from these forces. The focal injury may be coup (directly below the point of impact). Objects such as baseball bat, weapons, striking the front of the head usually produce only coup injuries (contusions and fractures) because the inner skull in the occipital area is smooth. Objects striking the back of the head usually result in both coup and countercoup injuries because of irregularity of the inner surface of the frontal bones. Objects striking the side of the head may produce coup of counter coup injuries. Brain edema forms around and in damaged neural tissues, contributing to the increasing ICP. Within the contused areas are infarction and necrosis, multiple hemorrhages, and edema. The tissue has a pulpy quality. The maximum effects of injury related to contusion, bleeding, and edema peak 18 to 36 hours after severe head injury.
31. Know most common primary CNS tumor
Pg. 613. Primary brain (intracranial) tumors, also called gliomas, comprise 50% to 60% of all adult brain tumors and include astrocytomas, oligodendrogliomas, mixed oligoastrocytomas, and ependymomas based on histologic and immunohistologic characteristics.
32. What happens to a patient after an acute spinal cord injury? Why is it life threatening? Describe the clinical manifestations. Why would their temperature fluctuate? Pg. 593. Normal activity of the spinal cord cells at and below the level of injury ceases because of loss of the continuous tonic discharge from the brain or brainstem and inhibition of suprasegmental impulses immediately after cord injury, thus causing spinal shock. Loss of all skeletal muscles, bladder vasoconstriction and increased metabolism. The individual assumes the temperature of the air.
33. Know diagnostic criteria for vegetative state and brain death. Pg.
A vegetative state has been called a wakeful unconsciousness state. 1)periods of eye-opening spontaneous or following stimulation; 2) The potential for sup cortical responses to external stimuli including generalized physiological responses to pain, Motor responses, such as grasp reflex; 3) return of so-called vegetative autonomic functions, including sleep wake cycles and normalizing of respiratory and digestive system functions; 4) occasional Roving eye movements without concomitant visual tracking ability. The persons eyes open spontaneously or following stimulation or both. There may be random and extremity or head movements. The individual maintains blood pressure and breathing without support. Brainstem reflexes pupillary oculocephalic, chewing swallowing are intact. No discrete localizing motor responses are present, and the individual does not speak any comprehensible words or follow commands. There is no awareness of self or the environment. Brain death occurs when irreversible brain damage is so extensive that the brain has no potential for recovery and no longer can maintain the bodies internal homeostasis. Destruction of the neuronal contents of the intracranial cavity includes the brainstem and cerebellum. On post mortal examination the brain is autolyzing, which is self digesting or already autolyzed. Criteria for brain death:
1) completion of all appropriate and therapeutic procedures 2) unresponsive coma absence of motor and reflex movements
3) no spontaneous respiration(apnea) PaCO2 that rises above 60 mmhg without breathing efforts, providing evidence of a nonfunctioning respiratory center (apnea challenge) 4) absent cephalic reflexes no ocular responses to head turn or caloric stimulation with dilated fixed pupils 5) Isoelectric flat EEG electro-cerebral silence
6) persistence of the signs for 30 minutes to one hour and for six hours after onset of coma and apnea 7) confirming test indicating absence of cerebral circulation
34. Define and discuss the different types of stroke, which affected artery causes what data processing deficits (agnosia, dysphasia, etc). Pg.
601-602. Thrombotic strokes arise from arterial occlusion caused by thrombi formed in the arteries supplying the brain or the intracranial vessels. The development of the cerebral thrombosis most frequently is attributed to atherosclerosis and inflammatory disease processes that damage arterial walls. Increased coagulation can lead to thrombus formation. Conditions causing inadequate cerebral perfusion dehydration hypotension prolonged vasoconstriction from malignant hypertension that increase the risk of thrombosis. The new definition of transient ischemia attack is a brief episode of neurologic dysfunction caused by of focal disturbance of brain or retinal ischemia with clinical symptoms typically lasting less than one hour and without evidence of infarction. And embolic stroke involves fragments that break from a thrombus formed outside the brain or in the heart aorta common carotid or thorax. Emboli infrequently arise from the ascending aorta or common carotid artery. The embolus usually involves small vessels and obstructs at bifurcation or other point of Narrowing thus causing ischemia. Hemorrhagic stroke is the third most common cause of CVA 10% of strokes and accounts for 10 to 15% of CVAs in white but 30% and blacks and Asians. The most common causes of spontaneous primary hemorrhagic stroke are hypertension ruptured aneurysms arteriovenous malformation and fistula amyloid angiopathy and cavernous angioma. Lacunae infarcts are caused by lipohyalinisis, subintimal lipid loading foam cells, and fibrinoid that thicken the arterial walls and are associated with smoking hypertension and diabetes mellitus. Because of the sub cortical location and small area of infarction these strokes may have pure motor and sensory deficits.
35. Know all types of cerebral edema and what causes each type. (Pg. 560, 6th edition) There are three types of cerebral edema:
•Vasogenic edema – caused by the increased permeability of the capillary endothelium of the brain after injury to the vascular structure disrupting the blood-brain barrier. Plasma proteins leak into the extracellular spaces, drawing water, and the water content of the brain parenchyma increases. Vasogenic edema starts in the area of injury and spreads with preferential accumulation in the white matter of the ipsilateral side because the parallel myelinated fibers separate more easily. Edema then promotes more edema because of ischemia from increasing pressure. •Cytotoxic (metabolic)
edema – Toxic factors directly affect the cellular elements of the brain parenchyma causing failure of the active transport systems. Cells lose potassium and gain sodium and water causing cellular swelling. Occurs mostly in the gray matter and may increase vasogenic edema. •Interstitial edema – often seen with noncommunicating hydrocephalus. Caused by transependymal movement of CSF from the ventricles into the extracellular spaces of the brain tissues. The brain fluid volume is increased predominantly around the ventricles. Hydrostatic pressure increases in the white matter, and the size of the white matter is reduced r/t rapid disappearance of myelin lipids.
36. Know characteristics of AV malformation. (Pg. 607, 6th edition) In an arteriovenous malformation (AVM), arteries feed directly into veins through a vascular tangle of malformed vessels. An AVM is a developmental abnormality that represents persistence of embryonic patterns of blood vessels, do not have a normal blood vessel structure, and are abnormally thin. They occur in any part of the brain, are cone-shaped, vary in size, may include the dura mater, and occur as frequently in males as females. They are typically present at birth but do not rupture until the second and third decades of life. Blood is shunted into the malformation depriving surrounding healthy tissue of adequate perfusion. Symptoms vary but may include: migraine, seizures, intracerebral/subarachnoid/or subdural hemorrhage, hemiparesis, sudden death.
37. Define and describe the pathophysiology, clinical manifestations and etiology of Multiple Sclerosis. (pg 630-632, 6th edition) *MS is an autoimmune disorder diffusely involving degeneration of CNS myelin and loss of axons. The PNS is not involved. It is diffuse and progressive, affecting the white and gray matter. *Patho/Etiology: MS is described as occurring when a previous viral insult to the nervous system has occurred in a genetically susceptible individual with a subsequent abnormal immune response in the CNS. The innate and adaptive immune systems are activated in MS. Early inflammation and demyelination lead to irreversible axonal degeneration and scarring or sclerosis. Demyelinated axons are more fragile and susceptible to further damage. Once degeneration exceeds self-repair, permanent damage results.
The immunopathology involves:
1. CD8+ T-cell activation (autoreactive), cells cross the blood-brain barrier and enter CNS and attach myelin 2. IL-12 and IL-23 (pro-inflammatory cytokines)
3. Lack of IL-10 (an anti-inflammatory cytokine)
4. IL-17 (pro-inflammatory cytokine)
5. Integrins expressed to facilitate to adherence and passage of immune cells into the CNS. 6. Chemokines promote the migration of immune cells and are up-regulated by MS 7. B lymphocytes and plasma cells contribute to the inflammatory response and directly damage myelin and axons, B cells are more active in chronic or progressive forms of MS 8. Complement activation (promotes inflammation) during the acute phase o, may be neuroprotective during relapse.
Eosinophil’s and neutrophils and macrophages are also present. The demyelination disrupts sodium, calcium, and potassium ion channels and calcium influx is proinflammatory and cytotoxic in itself. Activated microglia and macrophages release nitric oxide and oxygen free radicals Activated immune cells also produce glutamate, a neurotoxin.
MS is also characterized by focal inflammation and diffuse injury throughout the CNS (MS lesions). Box 17-8 (pg 632) describes pathologic patterns. Lesions may occur anywhere in white or gray matter. In addition, other neurodegenerative processes include: 1) changes in gray matter in the cortex, basal ganglia, brainstem, and spinal cord with substantial loss over time. 2) Brain atrophy that begins early in the disease and is highly correlated with disability and progressive MS. 3) Direct dysfunction of or damage to oligodendrocytes that manufacture myelin.
*Clinical manifestations: Infection, trauma, or pregnancy could all be precipitating events before the onset or exacerbation of symptoms. Most pregnancy related exacerbations occur 3 months postpartum, suggesting a relation to the stresses of labor and the increased fatigue during the postpartum period, rather than the pregnancy itself. The major classifications of MS are relapsing-remitting (90% of cases), primary progressive(10% of cases), secondary progressive, and progressive-relapsing. There are 3 established syndromes of MS:
Mixed (general) type: (50% of cases) – optic neuritis which causes impaired central vision, impaired color perception, decreased central visual acuity, defective pupillary response to light, optic papillitis, retrobulbar neuritis; internuclear ophthalmoplegia, diplopia, eyeball pain, tinnitus, deafness, facial weakness, vertigo, vomiting, nystagmus, dysarthria, decreased short term memory, decreased concentration, word finding problems , planning difficulties, recent memory impairment Spinal type: (30-40% of cases) – weakness/numbness in limbs, bladder/bowel dysfunction, neurogenic impotence, constipation Cerebellar type: (5% of cases) – motor ataxia, nystagmus, hypotonia, asthenia, Charcot triad (combo of dysarthria, intention tremor, and nystagmus), parasthesias, tonic head turning, Lhermitte sign (momentary parasthesia or tingling sensation that shoots down the trunk or limbs during neck flexion).
Etiology – 0.1% of the U.S. population is affected; onset between age 20-40, male:female ratio is 1:2, 15% of those with MS have an affected relative, multiple possible genes identified as cause – See pg 630 for further detail.
38. Define and describe the pathophysiology, clinical manifestations and etiology of Guillian Barre Syndrome. (Pg. 636 , 6th edition) Guillian Barre Syndrome – an acquired acute autoimmune demyelinating or axonal polyneuropathy with four subtypes: Acute inflammatory demyelinating polyneuropathy, Acute motor axonal neuropathy, Acute motor and sensory axonal neuropathy, Fisher syndrome (See table 17-14, Pg. 637 for further detail on subtypes)
Etiology – incident rate is 1-2 per 100,000 people; 4-6% mortality rate; 5-10% morbidity rate
Patho – GBS is an autoimmune disease triggered by a preceding bacterial or viral infection. The muscle innervated by the damaged peripheral nerves undergoes denervation and atrophy. If the cell body survives, regeneration of the peripheral nerve takes place and recovery of function is likely. If the cell body dies, no regeneration is possible. Collateral reinnervation from surviving axons may take place in which residual deficits persist.
Clinical manifestations – numbness, pain, paraesthesias, or weakness of limbs; dysphagia, dysarthria, tachycardia/bradycardia, hypotension/hypertension, loss or increase in sweating, respiratory arrest, cardiovascular collapse, hyponatremia.
39. Define and describe the pathophysiology, clinical manifestations and etiology of Mysthenia Gravis (Pg. 639, 6th edition) Myasthenia Gravis – a chronic autoimmune disease mediated by acetylcholine receptor antibodies that act at the neuromuscular junction.
Etiology – unknown
Patho – results from a defect in nerve impulse transmission at the neuromuscular junction mainly the formation of autoantibodies against receptors at the ACH binding site on the postsynaptic membrane. Eventually, the destruction of receptor sites occurs and the number of receptors on the plasma membrane is reduced diminishing the transmission of nerve impulses. Muscle depolarization is incomplete or not achieved. Subtypes include: neonatal myasthenia, ocular myasthenia, and generalized AChR myasthenia.
Clinical manifestations – fatigue & weakness that worsens with activity, improves with rest, and recurs with resumption of activity; an insidious onset of symptoms; diplopia, ptosis, ocular palsies, impaired swallowing, impaired chewing, an expressionless face, weight loss, aspiration, nasal voice, impaired ventilation,
40. Define and describe the pathophysiology, clinical manifestations and etiology of Parkinsons disease. (Pg. 572-574 , 6th edition) Parkinsons disease – commonly occurring degenerative disorder of the basal ganglia involving the dopaminergic (dopamine-secreting) nigrostriatal pathway.
Etiology – classification includes primary and secondary parkinsonism; onset occurs after 40 years old, equal incidence in sexes, 1-2% of the U.S. over age 60 is affected.
Patho – hallmark pathologic features are loss of dopamine pigmented neurons in the substantia nigra pars compacta with dopaminergic deficiency in the putamen portion of the striatum. Dopamine loss in other brain areas such as brainstem, thalamus, and cortex. Degeneration of the dopaminergic nigrostriatal pathway to the basal ganglia results in underactibity of the direct motor pathway and overactivity of the indirect motor loop (which normally inhibits movement). This results in inhibition of the motor cortex manifested with bradykinesia and rigidity.
Clinical Manifestations – insidious onset of symptoms; bradykinesia, resting tremor, muscle rigidity, hypoakinesia, postural abnormality, hyponosmia, fatigue, pain, autonomic dysfunction, sleep fragmentation, depression, and dementia with or without psychosis
41. Define and describe the pathophysiology, clinical manifestations and etiology of Huntington disease. (Pg. 570, 6th edition) Huntington disease – aka chorea; a relatively rare, hereditary-degenerative disorder diffusely involving the basal ganglia and cerebral cortex.
Etiology – onset at age 25-45 years old (the age of onset of symptoms is related to the length of the repeat sequences and mechanisms of toxitcity), prevalence rate of 2-8 people per 100,000 persons and occurs in all races
Patho – an autosomal dominant trait with high penetrance. The genetic defect is on the short arm of chromosome 4. There is an abnormally long polyglutamine tract in the Huntington protein that is toxic to neurons caused by a cytosine-adenine-guanine trinucleotide repeat expansion. The principle pathologic feature is severe degeneration of the basal ganglia, particularly the caudate and putamen nuclei, and the frontal cerebral cortex.
Clinical manifestations – abnormal movement and progressive dysfunction of intellectual processes (dementia) and thought processes, decreased short term memory, inability to plan/organize/or sequence, attention deficits, bradyphenia (slow thinking), apathy, restlessness, irritability, depression, euphoria
42. Prenatal and perinatal factors may result in what psychiatric condition? (Pg. 647, 6th edition) Schizophrenia: a leading hypothesis for the etiology of schizophrenia suggests that the illness results from neurodevelopmental defects that occur in fetal life. According to this hypothesis, environmental factors (viral infection during pregnancy, prenatal nutritional deficits, & perinatal complications) interfere with genetically programmed neural development leading to altered brain structure and function.
43. What is schizophrenia? What part of the brain is associated with the S/S of this disorder? (Pg. 647-650, 6th edition)
Schizophrenia – a collection of illnesses characterized by thought disorders. Thought disorders reflect a break between the cognitive and emotional sides of one’s personality. Divided into positive and negative symptoms. Positive – hallucinations, delusions, cognitive disorder, thought disorder, bizarre behavior. Negative – flat affect, alogia (lack of speech), anhedonia, attention deficits, and apathy. Schizophrenia has a strong genetic component involving several genes located on different chromosomes (example: chromosome 22q11). Early development may involve issues from environmental factors (viral infection, nutritional deficiencies, or prenatal birth complications) which may interfere with genetic programming of neural development leading to alterations in brain structure and function. Structural brain abnormalities present. Enlargement of cerebroventricles and widening of fissures and sulci in frontal cortex may occur. Reduction in the volume of the thalamus, disrupting communication among cortical brain regions, and the temporal lobe, which may be responsible for producing the positive symptoms. Frontal lobe has a progressive loss of volume and worsening of negative symptoms. Functional alterations in the dorsolateral
prefrontal cortex, (reduced blood flow and metabolism) compromise abilities to engage in goal-directed and cognitive problem-solving behavior. Dopamine levels are abnormal lending to the dopamine hypothesis (suggests that elevation in dopaminergic transmission contributes to the onset of schizophrenia). More current dopamine hypothesis views that dopamine pathways in the brain are altered. Another neurotransmitter system that may be involved is the excitatory neurotransmitter gluttamate and its actions on the N-methyl-D-aspartame receptor subtype.
44) Define depression and its types: Know etiology. (pg. 652-656)
When emotional states such as sadness, become predominant and uncontrollable, individuals may be diagnosed with a mood disorder called depression. The 2 major types of depression are: * Unipolar or Major Depressive Disorder consists of episodes of depression; most common mood disorder, which consists of episodes of depression. Unremitting feelings of sadness or despair, insomnia, loss of appetite, weight loss, reduced interest in pleasurable activities and interpersonal relationships, reduced motor activity, marked fatigue, decreased ability to concentrate, pessimistic attitude, suicidal thoughts.
* Bipolar Disorder, also known as manic-depressive illness that’s has two subtypes: * Bipolar I features manic episodes and at least one major depressive episode * mania is elevated levels of euphoria, elevated self esteem, enhanced energy levels, poor judgment, hypersexual, excessive, loud, rapid, and pressured speech. Some develop psychotic symptoms such as hallucinations or delusions.
* Bipolar II characterized by recurrent major depressive episode with one or more hypomanic (milder than manic) episodes.
Mood disorders have a strong tendency to run in families. Bipolar and schizophrenia are associated with loci on chromosome 18 and 22. However, large variation in clinical symptoms suggest that developmental and
environmental factors are as important as genetic factors in contributing to etiology of mood disorders. The interplay between life stressors and a potentially dysfunctional serotonin (5-HT) system appears to elevate the risk of depression. Depression occurs following a deficit in brain norepinephrine, dopamine, and/or serotonin.
45) How Does ECT (electroconvulsive therapy) treat depression? (pg. 658)
ECT is used when individuals fail to respond to antidepressants or when they are severely depressed, pregnant, suicidal, or psychotic. Mechanism of action of ECT is unclear, but the procedure is known to produce alterations in monoamine systems.
46) Define generalized anxiety disorder. What is the underlying defect? (pg. 660)
GAD is defined as excessive and persistent worries (at least six months). The individual worries about life events such as marital relationships, job performance, health, money, or social status. Six major symptoms: restlessness, muscle tension, irritability, easily fatigued, difficulty concentrating, and difficulty sleeping. Depression and substance abuse is a frequent complication of GAD. Abnormalities in norepinephrine and serotonin systems are reported in GAD. A prominent alteration involves the GABA-BZ receptors. There is a reduction in peripheral BZ receptors.
47) Define panic disorder. What are the complications? (pg. 659)
Panic disorder is a condition that consists of multiple disabling panic attacks. Between attacks, the individual spends an excessive amount of time worrying about the next panic attack. Panic attacks are characterized by intense autonomic arousal involving a wide variety of symptoms, including lightheadedness, racing heart, difficulty breathing, chest discomfort, sweating, generalized weakness, trembling, abdominal distress, chills, hot flashes, fear of losing control and dying. A notable complication of the disorder is the development of agoraphobia, avoidance of places or situations where escape or help is not readily available. Severe agoraphobia leads to the individual becoming house bound.
48) Define encephalocele, memingocele, spina bifida, myelomeningocele. Where is the defect located in each?
Encephalocele (pg. 669) : herniation or protrusion of brain and meninges through a defect in the skull, resulting in a saclike structure. Occurs during the first weeks of pregnancy, most occur in the occipital area, with others occurring in the parietal, frontal, or nasopharyngeal regions. Size, location, and involvement determine a child’s development and intellectual outcome.
Meningocele (pg. 669): Saclike cyst of meninges filled with spinal fluid located on the posterior arch of the vertebra. Develops during the first four weeks of pregnancy when the neural tube fails to close completely. Cystic dilation of meninges protrudes through the vertebral defect and around the malformed tube. The dura mater may be missing and the arachnoid layer of the meninges bulges beneath the skin. This defect DOES NOT involve the spinal cord, occur equally in the cervical, thoracic, and lumbar areas, clubbed foot, gait disturbances, bladder dysfunction, and upper extremity weakness may be present. Hydrocephalus is common.
Myelomeningocele (pg. 669-671): A hernial protrusion of a saclike cyst (containing meninges, spinal fluid, and a portion of the spinal cord with nerves) through a defect in the posterior arch in the vertebra. * Most are located on the lumbar or lumbosacral regions * failure of the neural tube to close, resulting in cystic dilation of meninges and protrusion of the spinal cord through vertebral defect * occurs during the first four weeks of pregnancy
* the sac may be intact or may be leaking CSF (increases risk for infection) * requires surgical intervention
* Life threatening complication is Arnold-Chiari type II malformation * involves the downward displacement of the cerebellum, cerebellar tonsils, brain stem, and fourth ventricle * the downward displacement of the above structures through the foramen magnum and into the cervical space exerts pressure on the 10 cranial nerves housed by the brainstem, which results in altered functions or palsies. * Hydrocephalus, seizures, visual and perceptual problems are common * motor and sensory functions below the level of the lesions ore altered, including weakness, paralysis, spasticity, bowel and bladder dysfunction * increased complications arise as the child grows: scoliosis, altered gait pattern, changes in muscle strength below the lesion, back pain, clubfoot, dislocation of hips, kyphosis, and disturbances in bowel or bladder patterns. These are associated with Tethered Cord Syndrome.
Spina Bifida (pg. 671): When defects of the neural tube occur, an accompanying vertebral defect allows the protrusion of the neural tube contents. Cause is unknown, however, linked to maternal folate deficiency. Most defects are located in the lumbosacral area, especially the 5th lumbar and 5th sacral vertebra when the posterior vertebra laminae have failed to fuse. * In spina bifida occulta, individual may have no serious dysfunctions * abnormal growth of hair along spine.
* midline dimple with or without a sinus tract.
* cutaneous angioma.
* subcutaneous mass representing a lipoma or dermoid cyst. * common defects include: gait abnormalities, positional deformities of the feet as a result of muscle weakness, sphincter disturbances of the bowel or bladder * surgical closure is usually completed in the neonatal period.
49) Know when the neural groove closes during embryonic development. ( pg 665)
During the fourth gestational week the neural groove deepens, its folds develop laterally, and it closes dorsally to form the neural tube, epithelial tissue that ultimately becomes the CNS.
50) Know pathophysiology, clinical manifestations and etiology of cerebral palsy. (pg 675-676)
Cerebral palsy is the term given to a diverse group of nonprogressive syndromes that affect the brain and cause motor dysfunction beginning in early infancy.
Low birth weight and birth asphyxia are commonly identified risk factors for cerebral palsy. Hypoxia and asphyxia are known to cause edema in the brain. Lack of oxygen and the incorporation of amino acids during protein synthesis lead t acidosis. Carbon dioxide and lactic acid accumulate with acidosis, causing osmotic pressure changes. This condition contributes to generalized cerebral swelling and CNS damage. See table 19-3 for predisposing factors and known causes.
Symptoms with cerebral palsy are associated with areas of brain that are damaged, pyramidal (spastic) and extrapyramidal (nonspastic). Pyramidal palsy results from damage or defects in the brain’s corticospinal pathways in either one or both hemispheres and accounts for about 70-80% of cerebral palsy cases. It is associated with increased muscle tone, prolonged primitive reflexes, exaggerated deep tendon reflexes, clonus, rigidity of extremities, scoliosis, and contractures. Cognitive impairment occurs in about 30 % of cases. Extrapyramidal palsy results from damage to cells in the basal ganglia, thalamus, or cerebellum and includes 2 subtypes : Dyskinetic and Ataxic. Dyskinetic Cerebral Palsy is associated with extreme difficulty in fine motor coordination and purposeful movement. Movements are jerky, uncontrolled, and abrupt resulting from damage to the basal ganglia or thalamus. Ataxic cerebral palsy is associated with damage to the cerebellum and manifests with gait disturbances and instability. Children with cerebral palsy have associated neurologic disorders, such as seizures, intellectual impairment, and visual impairment.
Table 19-3- cerebral palsy causes. (Easier to read there). (pg-676).
51) Know pathophysiology, clinical manifestations and etiology of PKU. (pg 677)
Pathophysiology and etiology:
PKU is an inborn error of metabolism characterized by inability of the body to convert the essential amino acid phenylalanine to tyrosine. PKU is caused by phenylalanine hydroxylase deficiency, phenylalanine hydroxylase controls the conversion of phenylalanine to tyrosine in the liver. The body uses tyrosine in the biosynthesis of protein, melanin, thyroxine, and the catecholamines in the brain and adrenal medulla. Its deficiency causes an accumulation of phenylalanine in the serum and subsequently in the urinary excretion of abnormal metabolites called phenyl acids. Such high levels of phenylalanine prevent sufficient neutral amino acid entry into brain, which contributes to the neuropathologic process of PKU. Brain damage occurs before metabolites can be detected in urine, and damage continues as long as phenylalanine levels remain high.
CM are related to CNS damage range from mild to severe behavioral disturbances, self-abusive tendencies, and seizures. Because of lack of tyrosine and in a relationship to biosynthesis of melanin, children with PKU have a characteristic phenotype that includes blond hair, blue eyes and fair skin. Children with genetically darker complextions may be red haired or brunette.
52) What nerves are capable of regeneration? (pg 445)
Myelinated fibers of Peripheral nervous system are capable of regeneration. A crushing injury allows recovery more fully than a cut injury.