Nu Patho Study Guide Unit 2

26.Know normal intracranial pressure. How does body compensate for increased ICP?

*NORMAL INTRACRANIAL PRESSURE (ICP) = 5-15mmHg OR 60-180 mm H₂O. The RED font indicates the compensatory mechanisms for ↑ ICP. Stage 1: Cerebral blood volume is altered which causes intracranial hypertension. Vasoconstriction and external compression of the venous system occur in an attempt to further decrease the intracranial pressure. Thus, the ICP may not change due to compensatory mechanisms {CSF is reduced through increased reabsorption. Blood volume is reduced by compression of intracranial veins.} 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.

36.Know characteristics of AV malformation

AV malformation (p.604-605) In an arteriovenous malformation, arteries feed directly into veins through a vascular tangle of malformed vessels without a true capillary bed. AVMs occur as frequently in males as in females, and occasionally are found in families. Although usually present at birth, AVMs exhibit a delayed age of onset and symptoms most commonly occur before 30 years of age. They usually rupture in the second or third decades of life. Pathophysiology AVMs are developmental abnormalities that represent persistence of embryonic patters of blood vessels, do not have a normal blood vessel structure, and are abnormally thin. Involved vessels enlarge over time, size highly variable, may involve dura matter including the falx cerebri and tentorium cerebelli, may be fed by one or several arteries, feeder vessels become tortuous over time and often dilated. Clinical Manifestation 20% of people with AVM have a characteristic chronic nondescript headache, although some experience migraine; 20-25% experience seizure disorders caused by compression. Initially, the seizures tend to be focal or Jacksonian; generalization often occurs over time. The other 40-70% suffer an intracerebral, a subarachnoid, or a subdural hemorrhage. Bleeding from an AVM into the subarachnoid space causes clinical manifestation identical to those associated with a ruptured aneurysm. If bleeding is into the brain tissue, focal signs that develop resemble a stroke-in-evolution. 10% of person experience hemiparesis or other focal signs. Hemiparesis usually is caused by compression or rupture. At times non-communicating hydrocephalus develops with a large AVM that extends into the ventricle lining. AVM accounts for up to 1% of all sudden deaths. Evaluation and Tx A systolic bruit over the carotid in the neck, the mastoid process, or (in a young person) the eyeball is almost always diagnostic of an AVM. CT, MRA, transcranial Doppler, and MRI are used in initial diagnosis, followed by arteriogram to identify feeding vessels. Treatment options are microsurgery, embolization, stereotactic radiosurgery, or combination of treatments.

4. What is the function of the CSF? Where is it produced? Where is it absorbed?

Cerebral Spinal Fluid (CSF) - function, where produced, where reabsorbed? (p.465-466) The function of the CSF is to protect the brain and spinal cord structures. The intracranial and spinal cord structures float in the CSF protecting them from jolts and blows. The buoyant properties of the CSF also prevent the brain from tugging on nerve roots and blood vessels. Most of the CSF is produced in the choroid plexuses in the lateral third and fourth ventricles. It is reabsorbed into venous circulation through the arachnoid villi. These are primarily located in the superior sagittal sinus.

50.Know pathophysiology, clinical manifestations and etiology of cerebral palsy.

Cerebral palsy - Pathophysiology, Clinical manifestations & Etiology(p. 670-672) Cerebral Palsy is the term given to a diverse group of nonprogressive syndromes that affect that brain and cause motor dysfunction beginning in early infancy. It is a disorder of movement, muscle tone, or posture that is caused by injury or abnormal development in the immature brain. Although cerebral palsy is by definition nonprogressive, its clinical manifestations change with growth and maturation of the child. Pathophysiology Several factors, alone or in combination, can produce brain damage that leads to cerebral palsy. Prenatal cerebral hypoxia, congenital malformations and placental pathology can contribute to the systemic degeneration of immature areas of the brain white matter and interfere with cell maturation. The severity of the damage depends on the gestational age at the time of the injury and the degree of injury sustained. Pyramidal/spastic CP results from damage or defects in the brains corticospinal pathways (upper motor Neuron) in either 1 or both hemispheres. Extrapyramidal/nonspastic CP caused by damage to the cells in the basal ganglia, thalamus, or cerebellum. Clinical manifestations The syndromes associated with cerebral palsy can be classified according to the areas of the brain that are damaged, pyramidal (spastic) and extrapyramidal (dyskinetic, ataxic, or hypotonic). Pyramidal/spastic cerebral palsy results from damage or defects in the brain's corticospinal pathways (upper motor neuron) in either one of both hemispheres and accounts for approximately 70% to 80% of cerebral palsy cases. It is associated with increased muscle tone, prolonged primitive reflexes, exaggerated deep tendon reflexes, clonus, rigidity of the extremities, scoliosis and contractures. Cognitive impairment occurs in about 30% of cases. Extrapyramidal/nonspastic is caused by damage to cells in the basal ganglia, thalamus or cerebellum and includes two subtypes: dyskinetic and ataxic. Dyskinetic is associated with extreme difficulty in fine motor coordination and purposeful movements. Ataxic is associated damage to the cerebellum and manifests with gait disturbances and instability. Children with cerebral palsy often have associated neurologic disorders such as seizures, intellectual impairment ranging from mild to severe and visual impairment. Pyramidal/spastic CP: spasticity, dyskinetic, ataxic, or hypotonic movements. Extrapyramidal/nonspastic CP: Dyskinetic cerebral palsy: extreme difficulty in fine motor coordination and purposeful movements.(Jerky, uncontrolled, abrupt. (20-25% of all CP cases) Ataxic cerebral palsy: gait disturbances and instability. Hypotonia at birth leading to stiffness of trunk muscles, inability to balance body position without support. (5% of all cases). Etiology (Table 19-3) Prenatal - Maternal include metabolic diseases, nutritional deficiencies, twins or multiple births, bleeding, toxemia, blood incompatibilities, exposure to radiation, infection premature labor. Prematurity, genetic factors, congenital anomalies of the brain. Perinatal - Anesthesia during labor and delivery, mechanical trauma during delivery, immaturity at birth, metabolic disorders, electrolyte disturbances. Postnatal - head trauma, infections, cerebrovascular accidents, toxicities, environmental toxins.

44.Define depression and its types; know etiology.

Depression - types and etiology(p. 647-652) When emotional states, such as sadness, become chronic and uncontrollable, individuals may be diagnosed with depression; there are two major classifications of mood disorder: major/clinical depression & bipolar disorder. Major depression o Most common mood disorder and the leading cause of disability in the US and throughout the world; intense and sustained unpleasant state of sadness and hopelessness Bipolar disorder o Bipolar I disorder features manic episodes and at least one major depressive episode. Bipolar II disorder is characterized by recurrent major depressive episodes with one or more hypomania. Symptoms of Depression—five or more symptoms present in a two week period with at least one symptom as either depressed mood or loss of interest or pleasure: 1. Depressed or irritable mood 2. Loss of interests and pleasure 3. Significant(>5%) weight gain or loss in a month 4. Insomnia or hypersomnia 5. Psychomotor agitation or retardation 6. Fatigue or loss of energy 7. Feelings of worthlessness or excessive guilt 8. Poor concentration or indecisiveness 9. Recent thoughts of death or suicide Symptoms of Manic Episode—three or more (four if mood only irritable) during distinct period of abnormally and persistently elevated, expansive, or irritable mood occurring for at least one week: 1. Elevated Mood 2. Irritable mood 3. Inflated self esteem 4. Decreased need for sleep 5. Excessive talking 6. Racing/crowded thoughts 7. Distractibility 8. Increase in goal-directed activity 9. Excessive risky activities Etiology Genetic and environmental influences! (Environmental triggers such as psychosocial stress can facilitate onset of depression to those with a genetic vulnerability.) Depression 1) Reduction in brain monoamine neurotransmission (monoamine hypothesis of depression, page 653, 6th Ed.) 2) Deficit of norepinephrine, dopamine and/or serotonin, 3) increased cortisol (increased plasma cortisol stays elevated throughout evening and early morning) 4) abnormal thyroid hormones 5) life stressors and potential dysfunction of serotonin (5-HT) elevates risk 6) persons with copies of two s alleles more than likely will develop major depression and have suicidal thoughts in response to stress 7) alterations in blood flow to prefrontal and limbic brain regions (amygdala = emotional behavior) Bipolar (Mania): 1. Elevated brain monoamine neurotransmission 2. Loci on chromosomes 18 and 22, also linked with schizophrenia and deficits in reelin expression linked to genetic loci located on chromosome 22 with susceptibility to schizophrenia. Found in both Depression and Bipolar Disorder: 1. Structural brain alterations: reduced frontal lobe and limbic system volumes NEUROCHEMICAL DYSREGULATION Monoamine Hypothesis of Depression ⇒ A deficit in the concentration of brain norepinephrine, dopamine, and or serotonin is the underlying cause of depression. Three major classes of antidepressants are MAOI's, TCAs, and SSRIs. Dietary consumption of trytophan and AMPT produces a rapid return to depression in those successfully treated. This is all neurochemical dysregulation. NEUROENDOCRINE DYSREGULATION Stress and HPA dysregulation ⇒ The HPA plays an important role in the response to stress. Chronic activation of the HPA system and elevated glucocorticoid secretion are found in the later percentage of people with major depression. Antidepressant drugs effective in normalizing HPA are associated with a food clinical response, whereas persist and dysregulation of the HPA system is related to continued depression or relapse. Hypothalmic-Pituitary-Thyroid Stress Dysregulation ⇒ Approximately 20-30% of persons with MDD have an altered HPT system. Individuals exhibit increased CSF levels of thyrotropin releasing hormone, blunted thyroid stimulating hormone response to TRH challenge, and decreased nocturnal rise in TSH level that normally occurs between midnight and early morning. Abnormalities in thyroid function are also observed in bipolar disorder, especially among individuals with rapid cycling. NEUROANATOMIC AND FUNCTIONAL ABNORMALITIES There's a widespread decrease in serotonin 5-HT1A receptor subtype binding in the frontal, temporal, and limbic cortex, and hippocampus. Structural abnormalities associated with mood disorders, especially in frontal and limbic regions such as the amygdala. There are also reports of reduced frontal lobe volume in depressed individuals and decreased or asymmetric temporal lobe volume with bipolar illness and depression.

17. Which part of the brain controls movement of the eye?

Eye movement - what part of eye controls(p.509, and Fig 16-13) occipital lobe pg 508, superior colliculi pg 459.. Superior colliculi (part of the Mid brain) are involved with voluntary and involuntary visual motor movement (e.g. ability of eyes to track movement) Six extrinsic eye muscles, attached to the outer surface of each eye, allow gross eye movements and permit the eyes to follow a moving object. The six extrinsic eye muscles and their controlling motor CN (Cranial Nerve): 1) Lateral rectus - rotates eye away from midline CN VI 2) inferior oblique - rotates eye upward and away from midline CN III 3) superior rectus - rotates eye upward and towards midline CN III 4) Medial rectus- rotates eye medially (towards midline, or nose) CN III 5) Superior oblique - rotates eyes downward and away from midline CN IV 6) Inferior rectus - down and towards midline CN III

38.Define and describe the pathophysiology, clinical manifestations and etiology of Guillian Barre Syndrome.

Guillain-Barre Syndrome - Pathophysiology, Clinical Manifestations & Etiology(p. 622-624) An acquired acute inflammatory demyelinating or axonal polyneuropathy with four subtypes: Acute inflammatory demyelinating polyneuropathy, acute motor axonal neuropathy, acute motor and sensory axonal neuropathy, and fisher syndrome (only 5% of cases). Pathophysiology Considered to be an autoimmune disease triggered by a preceding bacterial or viral infection (Etiology). Molecular mimicry (cross-activation of self-epitopes and pathogen-derived peptides by autoreactive T and B cells) is associated with the immune injury. Glycolipids, particularly gangliosides, are immune targets. 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 from intense root involvement in the inflammatory-degenerative process, no regeneration is possible. Collateral reinnervation from surviving axons and regenerating axons may take place. In this case, motor recovery is less complete and residual deficits persist. Clinical Manifestations Vary depending on subtype. Typically first manifestations include numbness, pain, paresthesias, or weakness of the limbs. Motor signs manifest as an acute or subacute progressive paralysis. Proximal muscles may be involved earlier and more significantly than distal muscles. Paresis/Paralysis may be in an ascending pattern, involving the limbs, respiratory muscles, and bulbar muscles. Only bulbar muscles may be involved resulting in dysphagia and dysarthria. Weakness plateaus or improves by the fourth week in 90% of cases. Sensory symptoms include: paresthesias/dysthesias, tingling, burning, shocklike sensations (particularly in the limbs), pain, and numbness. Respiratory muscle weakness leads to vent support in 10-30% of cases. Cranial nerve weakness involves chewing, swallowing and coughing. Autonomic dysfunction shows as tachycardia, or bradycardia, hypo or hypertension, loss of or significant sweating. May undergo a respiratory or cardiac arrest. Hyponatremia caused by SIADH is also common. Diagnosis & Treatment Major diagnostic tests are CSF fluid examination, nerve conduction studies, and EMG. CSF shows high protein level (500mg/dl) without cellular abnormality. Nerve conduction studies help identify the subtype. Ventilatory support and management of the autonomic nervous system dysfunction are the two dominate aspects of therapeutic management. Intravenous immunoglobulin, plasmapheresis, or plasma exchanges or combination therapy with the first 2 weeks of onset of clinical manifestations may be indicated. After the disorder begins to remit, aggressive rehabilitation should be instituted.

37.Define and describe the pathophysiology, clinical manifestations and etiology of Multiple Sclerosis.

Multiple Sclerosis - Pathophysiology, Clinical manifestations, & Etiology (p. 619-620) MS is a chronic inflammatory disease involving degeneration of CNS myelin, scarring or formation of plaque, and loss of axons. MS is caused by an autoimmune response to self-antigens in genetically suceptible individuals. The onset is usually between 20 and 40 years of age with a peak of age 30. MS is the most prevalent CNS demyelinating disorder and a leading cause of neurologic disability in early adulthood. The etiology is unknown. Genetic and environmental factors and interactions are implicated in disease onset. A genetic link exists in the human leukocyte antigen (HLA) complex. Vitamin D deficiency, cigarette smoking, and Epstein-Barr virus infection are environmental risk factors. The first demyelinating event, or "clinically isolated syndrome (CIS), is a single episode of neurologic dysfunction lasting greater than 24 hours that can be a prelude to MS. Characteristic episodes include optic neuritis, solitary brainstem lesions, and transverse myelitis. Pathophysiology MS is a diffuse and progressive CNS disease that affects white and gray matter. Autoreactive T and B cells recognize myelin autoantigens and trigger inflammation in the CNS, leading to the loss of myelin sheaths and nerve conductivity and subsequently to the death of neurons. MS is described as occurring when a previous infectious insult to the nervous system has occurred in a genetically susceptible individual with a subsequent abnormal CNS immune response. Various mechanisms cause irreversible tissue damage (inflammation, oligodendrocyte injury, demyelination, scarring or plaque formation, and axonal degeneration) that characterizes MS. These degenerative processes begin early in the course of the disease and continue to progress throughout a person's life. Demyelinated axons are more fragile and susceptible to further damage and, when degeneration exceeds self-repair ability (remyelination), permanent disability results. Myelin destruction and axonal damage begin before symptom onset (early inflammatory demyelination). The innate and adaptive immune systems are activated in the pathology of MS. The immunopathology of MS involves the following events: Immunopathology 1. Activation of CD4+ and CD8+ T cells; cells cross the blood-brain barrier and enter the CNS and attack myelin 2. Production of interlukin (IL-12) and IL-23 (pro-inflammatory cytokines) 3. Lack of IL-10 (an anti-inflammatory cytokine) 4. Production of IL-17 (pro-inflammatory cytokine) by Th17 cells 5. Expression of Integrins expressed to facilitate adherence and passage of immune cells into the CNS. 6. Promotion of Chemokine migration of immune cells and are up-regulated in MS 7. Contribution of B lymphocytes and plasma cells to the inflammatory response and direct damage myelin and axons, B cells are more active in chronic or progressive forms of MS ( B cells produce autoantibodies, secrete inflammatory cytokines, and activate T cells by presenting antigen) 8. Activation of complement (promotes inflammation) during the acute phase, may be neuroprotective during relapse 9. Presence of cells of inflammation including eosinophils, neutrophil, and macrophages 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, primary progressive, secondary progressive, and progressive-relapsing. There are 4 established syndromes: mixed, spinal, amaurotic, and cerebellar. • Mixed (general) type (50% of persons) ⇒ Optic signs are optic neuritis. Brain stem signs are internuclear ophthalmoplegia, diplopia, vertigo, vomiting, nystagmus, dysarthria. Cerebellar signs are usually involved with all four limbs and has a spastic/ataxic gait and ataxia of the arms. • Spinal type (30-40% of persons) ⇒ Spastic ataxia, deep sensory changes in the extremities, bladder and bowel symptoms. • Cerebellar or Pontobulbar - Cerebral Type (5% of persons) ⇒ Motor ataxia, hypotonia, asthenia. • Amaurotic forms (5% of persons) ⇒ Blindess. Treatment Main treatment goal is to prevent permanent neurological damage and treat the symptoms. Symptoms management for fatigue, weakness, vertigo, ataxia, tremor, heat intolerance, spasticity, bladder dysfunction, bowel dysfunction, sexual dysfunction, sensory sensations, pain, cognitive difficulties, depression, and psychosocial issues is essential.

49.Know when the neural groove closes during embryonic development.

Neural groove closure in embryonic development(p. 660) The central nervous system develops from a dorsal thickening of the ectoderm known as the neural plate. This plate appears around the middle of the third gestational week and unfolds to form a neural groove and neural folds. During the FOURTH gestational week then neural groove deepens, its folds develop laterally, and it closes dorsally to form the neural tube, epithelial tissue that ultimately becomes the CNS. The neural tube closes first in the cervical region and then "zippers" in two directions - cranially and caudally.

11.What are the two types of fibers that transmit the nerve action potentials generated by excitation of any of the nociceptors.

Nociceptor excitation generating nerve action potentials - two types of nerve fibers that transmit these action potentials (p.486) 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 in initiating rapid reactions to stimuli (fast pain). (2) The small unmyelinated C fibers are polymodal and are stimulated by mechanical, thermal, and chemical nociceptors. They are responsible for the transmission of the diffuse burning or aching sensation that follow (slow pain).

9. Know different clinical descriptions of pain (acute, chronic, neuropathic); pain threshold/tolerance

Pain - clinical descriptions of pain; pain threshold/tolerance (p.491) CATEGORIES OF PAIN (Box 16-2) I. Neurophysiologic pain A. Nociceptive pain 1. Somatic - superficial, arising from connective tissue, muscle or bone, and skin; either sharp and well-localized (esp fast pain carried by A-delta fibers), or dull, aching, throbbing, and poorly localized as seen in polymodal C fiber transmissions. 2. Visceral - pain in internal organs and lining of body cavities w/ aching, gnawing, throbbing, or intermittent cramping quality. Transmitted by sympathetic afferents and is poorly localized b/c of the lesser # of nociceptors in visceral structures. Assoc. w/ N/V, hypotension, restlessness, and in some cases, shock. 3. Referred - Pain 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. B. Neuropathic (non-nociceptive) 1. Central pain (lesion/dysfunction in brain or spinal cord) 2. Peripheral pain (lesion/dysfunction in peripheral nervous system [PNS]) II. Neurogenic pain A. Neuralgia (pain in distribution of nerve) B. Constant 1. Sympathetically independent 2. Sympathetically dependent III. Temporal pain (time-related) A. Acute pain - A protective mechanism that alerts the individual to a condition or experience that is immediately harmful to the body 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. B. Chronic - 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. IV. Regional pain A. Abdominal pain B. Chest pain C. Headache D. Low back pain E. Orofacial pain F. Pelvic pain G. Joint pain V. Etiologic pain A. Cancer pain B. Dental pain C. Inflammatory pain Pain threshold/tolerance (p.491) Pain threshold is 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; intense pain at one location may cause an ↑ in threshold in another location. For example, a person w/ severe pain in one knee is less likely to experience chronic back that is less intense; this is called perceptual dominance. Pain tolerance is the duration of time or intensity of pain that an individual will endure before initiating overt pain responses and is generally ↓ w/ repeated exposure to pain; may be ↑ by alcohol consumption, persistent use of pain medication, hypnosis, warmth, distracting activities, and strong beliefs or faith.

3. Where is the primary defect in Parkinsons disease and Huntingtons?

Parkinson Disease, where is the primary defect? (p.564) The main disease feature is degeneration of the basal ganglia (corpus striatum, globus pallidus, subthalmic nucleus, and substantia nigra) involving the dopaminergic nigrostriatal pathway. Huntington Disease - where is the primary defect? (p.562) The principal pathologic feature of HD is severe degeneration of the basal ganglia, particularly the caudate and putamen nuclei and the frontal cerebral cortex. The degeneration of the basal ganglia leaves enlarged lateral ventricles.

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?

Spinal cord injury - what happens to patient immediately after, why it's life-threatening, clinical manifestations, why temperature would fluctuate (p. 589-594) The pathophysiological cascade of secondary spinal cord injury begins within a few minutes after injury. 1.) Microscopic hemorrhages appear in the central gray matter and pia arachnoid that increase size within 2 hours. 2.) Edema in the white matter occurs, impairing the microcirculation of the cord. 3.) Localized hemorrhaging and edema therefore are followed by loss of auto regulation, vasospasm, impaired venous drainage, and reduced vascular perfusion with development of ischemic areas. 4.) Tissue necrosis occurs and leads to disruption of myelin, axonal degeneration, and ischemic endothelial injury. 5.) Chemical and metabolic changes in spinal cord tissues produce further ischemia, vascular damage, and necrosis of tissues (auto destruction) by release of toxic excitatory amino acids, accumulation of endogenous opiates, lipid hydrolysis with production of active metabolites, and local free radical release. 6.) Circulation in the white matter tracts of the spinal cord returns to normal in about 24 hours, but gray matter circulation remains altered. 7.) There is proliferation of microglia and changes in astrocytes, and red cells begin to disintegrate, and resorption of hemorrhages begins. 8.) Degenerating axons are engulfed by macrophages in the first 10 days after injury. 9.) A cyst with fluid forms, and the traumatized cord is replaced by acellular collagenous tissue (a scar) usually in 3-4 weeks. 10.) Meninges thicken as part of the scarring process. Why is it life threatening? In the cervical region, cord swelling, may be life threatening because of the possibility of resulting impairment of the diaphragm function (phrenic nerves exit C3-C5) and vegetative functions mediated by the medulla oblongata. Clinical manifestations of acute spinal cord injury: Following spinal cord injury, loss of normal cellular activity below the site of injury ensues following the disruption of the tonic (continuous) discharge from the brain. Inhibition of suprasegmental impulses immediately following the injury causes spinal shock. Spinal shock is characterized by the complete loss of reflex function in all areas below the injury (lesion), and involves all skeletal muscles, bladder, bowel, sexual function, and autonomic control. Spinal shock may last for 7 to 20 days or as little as a few days or as long as 3 months. Signs that spinal shock is resolving include the reappearance of reflex activity, hyperreflexia, spasticity, and reflex emptying of the bladder. Severe injury to the spinal cord will result in obvious changes below the lesion including: paralysis and flaccidity in muscles, absence of sensation, loss of bladder and rectal control, transient drop in blood pressure and poor venous circulation. Flexion reflexes return first involving the toes, feet, then legs. Injury to the cervical and upper thoracic cord may result in a condition called neurogenic shock in addition to spinal shock. Neurogenic shock results from the loss of sympathic outflow causing vasodilation, hypotension, bradycardia and hypothermia. Autonomic hyperreflexia (dysreflexia) may develop following resolution of spinal shock and is associated with massive uncompensated cardiovascular response to stimulation of the sympathic nervous system. Dysreflexia is characterized by paroxysmal hypertension (systolic up to 300mmHG), pounding headache, blurred vision, sweating above the lesion with flushed skin and bradycardia. Dysreflexia is elicited by stimulation of sensory receptors below the site if injury (i.e. distended rectum or bladder). Temperature fluctuation: Following spinal cord injury relates to damage of the sympathic nervous system that causes faulty control of sweating and radiation through capillary dilation. The hypothalamus cannot regulate body heat through vasoconstriction and increased metabolism; therefore, the individual assumes the temperature of the air.

34.Define and discuss the different types of stroke, which affected artery causes what data processing deficits (agnosia, dysphasia, etc).

Stroke - types & which affected artery causes which data processing deficits (p. 598-603) CVAs are classified according to pathophysiology and thus are ischemic (thrombotic or embolic), global hypoperfusion (shock), or hemorrhagic. Thrombotic stroke -Arise from arterial occlusions caused by thrombi formed in arteries supplying brain or in the intracranial vessels. Attributed to atherosclerosis and inflammatory disease processes (arteritis) that damage arterial walls. Increased coagulation can form a thrombus. Conditions causing inadequate cerebral perfusion (dehydration, hypotension, prolonged vasoconstriction) increase risk. Clots form occluding artery and break off and travel up the vessel to distant sites where occlusion occurs producing stroke. TIA (transient ischemic attack) brief episode of neurologic dysfunction caused by focal disturbance of brain or retinal ischemia with symptoms lasting less than 1 hour without evidence of infarction. TIA represent thrombotic particles causing intermittent blockage. Embolic Stroke—Involves fragments that break from a thrombus formed outside brain or heart, aorta, common carotid or thorax. Emboli infrequently arise from ascending aorta or common carotid artery. Embolus involves small vessels and obstructs at bifurcation thus causing ischemia. Embolus may plug lumen entirely and break fragments that move up the vessel. High risk sources are atrial fibrillation, left ventricular aneurysm or thrombus, left atrial thrombus, recent MI, rheumatic valvular disease, mechanical prosthetic valve, non bacterial endocarditis, bacterial endocarditis, patent foramen ovale, and intracardiac tumors. Hemorrhagic Stroke: (intracranial hemmorage ICH)—Causes hypertension, ruptured aneurysms, arteriovenous malformation and fistula, amyloid angiopathy, and cavernous angioma. ICH can be secondary to TBI, bleeding into the ischemic brain infarction or tumor, or a bleeding disorder or anticoagulation. Risk factors hypertension, previous cerebral infarct, coronary artery disease and diabetes mellitus. Hypertensive hemorrhage usually occurs within the brain tissue. Mass of blood is formed and its volume increases. Hemorrhages are described as massive, small, slit, or petechial. Massive is several centimeters in diameter, small 1-2 cm . slit lies in subcortical area and petechial size of a pinhead bleed. Most common sites in the putamen of basal ganglia, the thalamus, the cortex and subcortex, the pons, caudate and cerebellar hemispheres. Lacunar Stroke: (lacunar infarct)—Is a microinfarct smaller than 1 cm and involves small perforating arteries, predominantly in the basal ganglia, internal capsules, and pons. Caused by lipohyalinosis, subintimal lipid-loading foam cells, and fibrinoid materials that thicken arterial walls and are associated with smoking, hypertension, and diabetes. These strokes may have pure motor and sensory deficits. Clinical Manifestations of Stroke: ischemic strokes vary depending on artery obstructed; Hemorrhagic strokes vary location and size of bleed. Focal defects in 80% altered consciousness 50%. Acute stroke treatment: "time is brain" ⇒Treatment needs to begin within 6 hours of symptom onset.

28.What is responsible for the tremors associated with Parkinsons Disease?

Tremors in Parkinson's (what is responsible?) (p. 567) The Parkinson tremor appears to result from instability of feedback from the basal ganglia to the cerebral cortex caused by the 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. When the individual performs voluntary movements, the tremor becomes temporarily blocked because other motor control signals arriving in the thalamus override the abnormal basal ganglia signals.

21.Know vomiting with which CNS injuries.

Vomiting with CNS injuries (p.533) Yawning, vomiting, and hiccups are complex reflex-like motor responses that are integrated by neural mechanisms in the lower brainstem. These responses may be produced by compression or diseases that involve tissues in the medulla oblongata. Such disorders include infection, neoplasm, or infarct. Similar responses are produced by dysfunction in the lower brainstem through direct stimulation. Vomiting with no associated nausea indicated direct involvement of the central neural mechanism (or pyloric obstruction). Vomiting is associated particularly with CNS injuries that (1) involve the vestibular nuclei (located in the lower pons and medulla oblongata) or their immediate projections, particularly when double vision (diploplia) also is present; (2) impinge directly on the floor of the fourth ventricle; or (3) produce brainstem compression secondary to increased intracranial pressure.

2. Know the function of the arachnoid villi.

Arachnoid villi - function (p.466) Arachnoid villi protrude from the arachnoid space, through the dura mater and lie within the blood flow of the venous sinuses. CSF is reabsorbed by means of a pressure gradient between the arachnoid villi and the cerebral venous sinuses. The villi function as one-way valves directing CSF outflow into the blood but preventing blood flow into the subarachnoid space. Thus CSF is derived from the blood, and after circulating throughout the CNS, it returns to the blood.

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?

Brain anatomy - (REVIEW THE ANATOMY OF THE BRAIN, THIS IS PROBABLY NOT ALL-INCLUSIVE TO THE TEST QUESTIONS). Keeping you awake? (p.457) The pineal body of the epithalamus has connections and functions closely associated with those of the limbic system. For example, the hormones of the pineal body have been show to influence reproductive ability, and the secretion of melatonin. The pineal body (a component of the epithalamus) secretes melatonin, which maintains circadian rhythms and the sleep-wake cycle. The reticular formation (a large network of connected tissue nuclei, or nerve cell bodies, within the brainstem) regulates vital reflexes such as cardiovascular function and respiration, it is ALSO essential for maintaining wakefulness, and in conjunction w/ the cerebral cortex is referred to as the reticular activating system. (p.454, under CNS 1st paragraph). Controlling thought? (p.456) The prefrontal area is responsible for goal-oriented behavior (i.e. ability to concentrate), short-term or recall memory, and elaboration of thought and inhibition on the limbic (emotional) areas of the CNS. Controlling speech? (p.457) 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, commonly as a result of a CVS, results in the inability to form, or difficulty in forming, words. Controlling emotions & behavior? (p.459) The hypothalamus functions fall into two major areas: maintenance of a constant internal environment and implementation of behavioral patterns. Integrative centers control ANS function, regulation of body temp., endocrine function, and regulation of emotional expression. The Limbic System principal effects are believed to be involved with primitive behavioral responses, visceral reaction to emotion, feeding behaviors, biologic rhythms, and the sense of smell. Expression of affect (emotional and behavioral states) is mediated by extensive connections with the limbic system and prefrontal cortex (p.457). Maintaining balance and posture? (p.459) The cerebellum is responsible for conscious and unconscious muscle synergy and for maintaining balance and posture. This is accomplished through extensive neural connections from the spinal cord and medulla oblongata through the inferior cerebellar peduncle and with the midbrain and higher structures through the superior cerebellar peduncle. One of the temporal lobe's secondary functions is balance. (p. 457)

18.What part of the brain must be functioning for cognitive operations?

Brain areas that must be functioning for cognitive operations(p. 527-550) 1. Attentional systems that provide arousal and maintenance of attention over time; 2. Memory and language systems by which information is communicated; 3. Affective or emotive systems that mediate mood, emotion, and intention. Full Consciousness is a state of awareness both of oneself and of the environment and appropriate responses to that environment. Consciousness has two distinct components: ~Arousal (state of awakeness) is mediated by the reticular activating system(RAS), which regulates aspects of attention and information processing and maintains consciousness. Cognitive cerebral functions require a functioning RAS. ~Awareness (content of thought) encompasses all cognitive functions including awareness of self, environment, and affective states (i.e. moods); mediated by the core networks (selective attention and memory) under the guidance of executive attention networks (i.e. the networks that involve abstract reasoning, planning, decision making, judgment, error correction, and self-control). *Not localized in a single brain area but is a network of interconnected brain circuits. Function and Disfunction: Selective attention (orienting) - ability to select specific information to be processed from available, competing environmental and internal stimuli and to focus on those stimuli ⇒ Frontal and parietal regions of right hemisphere contribute to selective attention; the engage component is mediated by the right parietal lobe; the move component is mediated by the superior coliculi for visual orienting. A weak orienting network = neglect syndrome. Sensory inattentiveness - a form of neglect and may be visual, auditory, or tactile; person may is able to recognize individual sensory input from the dysfunctional side when asked, but ignores (neglects, extinguishes) the sensory input from the dysfunctional side from stimulated from both sides - this phenomenon is called extinction. Entire complex of denial of dysfunction, loss of recognition of one's own body parts, and extinction is sometimes referred to as unilateral neglect syndrome, and is common after stroke. *No specific area of brain indicated in textbook. Selective attention deficit (orientation) - manifests as neglect syndrome rarely occurs b/c other deficits are present; may appear temporarily from a seizure activity or postictal state. Temporary or permanent deficits may occur with contusions or subdural hematomas, encephalitis, and ischemic stroke. Progressive neglect deficits may be found with gliomas or metastatic tumor and in Alzheimer's and Pick disease. Memory - the recording, retention, and retrieval of knowledge. Two types: declarative and nondeclarative. Declarative = involves learning and remembrance of episodic memories (personal hx, events, experiences) and semantic memories (facts and info); mediated by domain-specific cortical areas of association areas including 1) areas of temporal, parietal, and occipital lobes, where long-term memories are thought to be stores, 2) domain-independent areas of the medial temporal lobe (i.e. hippocampus), the diencephalon (thalamic structures and hypothalamus), and the basal forebrain (located ventral to the striatum and produces acetylchoine). Non-declarative memory (nonconscious) aka reflexive, procedural, or implicit memory, is of actions, behaviors (habits), skills, and outcomes. It is a motor memory, as it involves construction of the motor pattern for the motor performance so that the action, behavior, or skills becomes increasingly more automatic ⇒ striatum of the basal ganglia. Emotional memory - amygdala, located on inner surface of temporal lobe. Dysmnesia - disorder of the domain-independent declarative memory network; loss of past memories (retrograde amnesia) coupled with an inability to make new memories (anterograde amnesia) ⇒ hippocampus and other temporal lobe structures are often involved. Detection - recognition of object's identity and the realization of that the object fulfills a goal ⇒ anterior cingulate cortex, basal ganglia and other frontal areas function in color, motion, and form detection. Akinetic mutinism - a person can neither speak or move and exemplifies a detection deficit from disease or injury to the frontal lobe. Looking back at brain anatomy: Keeping you awake? (p.457) The pineal body of the epithalamus has connections and functions closely associated with those of the limbic system. For example, the hormones of the pineal body have been show to influence reproductive ability, and the secretion of melatonin. The pineal body (a component of the epithalamus) secretes melatonin, which maintains circadian rhythms and the sleep-wake cycle. The reticular formation (a large network of connected tissue nuclei, or nerve cell bodies, within the brainstem) regulates vital reflexes such as cardiovascular function and respiration, it is ALSO essential for maintaining wakefulness, and in conjunction w/ the cerebral cortex is referred to as the reticular activating system. (p.454, under CNS 1st paragraph). Controlling thought? (p.456) The prefrontal area is responsible for goal-oriented behavior (i.e. ability to concentrate), short-term or recall memory, and elaboration of thought and inhibition on the limbic (emotional) areas of the CNS. Controlling speech? (p.457) 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, commonly as a result of a CVS, results in the inability to form, or difficulty in forming, words. Controlling emotions & behavior? (p.459) The hypothalamus functions fall into two major areas: maintenance of a constant internal environment and implementation of behavioral patterns. Integrative centers control ANS function, regulation of body temp., endocrine function, and regulation of emotional expression. The Limbic System principal effects are believed to be involved with primitive behavioral responses, visceral reaction to emotion, feeding behaviors, biologic rhythms, and the sense of smell. Expression of affect (emotional and behavioral states) is mediated by extensive connections with the limbic system and prefrontal cortex (p.457).

5. Review blood flow to the brain.

Brain blood flow (p.467-469) The brain receives about 20% of the cardiac output. Carbon dioxide serves as a primary regulator for blood flow within the CNS as it is a potent vasodilator. The brain derives its arterial supply from two systems: the internal carotid arteries and the vertebral arteries. • Internal Carotid Arteries: o The ICAs supply blood to the anterior portion of the brain. They originate from the common carotid arteries, enter the cranium through the base of the skull, and pass through the cavernous sinus; after giving off some small branches, they divide into the anterior and middle cerebral arteries. • Vertebral Arteries: o The VAs supplies the posterior portion of the brain. They originate as branches off the subclavian arteries, pass through the transverse foramina of the cervical vertebrae, and enter the cranium through the foramen magnum. They join at the junction of the pons and medulla oblongata to form the basilar artery. • Basilar Artery: o 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 cerebellar artery, off the vertebral artery; and the anterior inferior cerebellar and superior cerebellar arteries, off the basilar artery. The basilar artery also gives arise to small pontine arteries. The large arteries on the surface of the brain and their branches are called superficial arteries. The small branches that project into the brain are termed projecting arteries. • Circle of Willis: o A structure credited with the ability to compensate for reduced blood flow from any one of the major contributors. Formed by the posterior cerebral arteries, posterior communicating arteries, internal carotid arteries, anterior cerebral arteries, and anterior communicating artery. *Cerebral venous drainage does NOT parallel its arterial blood supply; whereas the venous drainage of the brainstem and the cerebellum DOES parallel the arterial supply of the structures. The veins drain into the venous plexuses and dural sinus and eventually join the internal jugular veins at the base of the skull.

20.Know the best prognostic indicator of recovery of consciousness and functional outcome after a brain event.

Brain event/injury - best prognostic indicator of recovery of consciousness and functional outcome(p. 533, 582, 584, 587-588) Evaluation is based on history, LOC using the Glasgow Coma Scale, imaging (CT, MRI, PET), and assessment of vital parameters (ICP and EEG). (p. 584) Glasgow Coma Scale (used to assess severity of injury); *hallmark of severe TBI is loss of consciousness for 6 hours or more. (1) Mild TBI w/ mild concussion = score of 13-15; (2) moderate TBI w/ structural injury such as hemorrhage or contusion = score of 9-12; (3) severe TBI w/ cognitive and/or physical disability or death = score of 3-8. (p.582) An isoelectric, or flat, EEG (electrocerebral silence) for 6-12 hours in a person who is not hypothermic and has not ingested depressant drugs indicates that no mental recovery is possible; the brain is dead (p.533). Alterations in arousal - determine extent of brain dysfunction and identify ↑ or ↓ CNS function: Level of consciousness - most critical clinical index of nervous system function/dysfunction. Pattern of breathing - evaluates level of brain dysfunction; rate, rhythm, and pattern should be assessed. Pupillary changes - valuable guide to evaluate presence/level of brainstem dysfunction Oculomotor responses - resting, spontaneous, and reflexive eye movements and oculovestibular (caloric) reflexes change at various levels of brain dysfunction (Caloric Ice-Water test, Fig 17-4 p. 533). (*All of these are on p. 528-533) Motor responses - evaluates the level of brain dysfunction and determining side of brain that is maximally damaged; responses may be purposeful, inappropriate, or not present.

31.Know most common primary CNS tumor.

CNS tumor (most common primary CNS tumor) (p. 629-630) Astrocytomas are a type of glioma and the most common primary CNS tumor (50% of all brain and spinal cord tumors). Astrocytomas develop from astrocytes and grow by expansion and infiltration into the normal surrounding brain tissues. Tumor cells are believed to have lost normal growth restraint, and thus they proliferate uncontrollably. These slow-growing but infiltrative gliomas tend to form cavities (pseudocysts). Although these tumors may occur anywhere in the brain or spinal cord, they are located most commonly in the cerebrum, hypothalamus, and pons. Headache and subtle neurobehavioral changes may be an early symptom. Approximately half of persons with low-grade astrocytomas experience a focal or generalized seizure. There are four grades: I, II, III, IV. Diagnosis of high-grade astrocytomas most commonly takes 3-6 mos. From onset on the first clinical manifestation because the person does not recognize the need to consult a healthcare provider.

35.Know all types of cerebral edema and what causes each type.

Cerebral edema - types and causes of each (p.557-558) an increase in the fluid content of brain tissue, a net accumulation of water within the brain. Three types of cerebal edema 1. Vasogenic edema: clinically the most common type. It is caused by the increased permeability of the capillary endothelium of the brain after injury to the vascular structure. The result is a disruption in the blood-brain barrier. Vasogenic edema start in the area of injury and spread with preferential accumulation in the white matter of the ipsilateral side because the parallel myelinated fibers separate more easily. 2. Cytotoxic (metabolic) edema: toxic factors directly affect the cellular elements of the brain parenchyma (neuronal, glial and endothelial cells) causing failure of the active transport systems. The blood-brain barrier is not disrupted. The cells lose their potassium and gain larger amounts of sodium. Water follows by osmosis into the cells so that the cells swell. Cytotoxic edema occurs principally in the gray matter and may increase vasogenic edema. 3. Interstitial edema: seen most often with non-communicating hydrocephalus. The edema is caused by transependymal movement of CSF from the ventricles into the extracellular spaces of the brain tissues. The brain fluid volume this is increased predominately around the ventricles. The hydrostatic pressure within the white matter increases and the size of the white matter is reduced because of the rapid disappearance of myelin lipids.

23.Know the characteristics of closed head injury.

Closed head injury - characteristics(p.582) Closed (blunt) trauma is more common and involves either the head striking a hard surface or a rapidly moving object striking the head. The Dura mater remains intact, and brain tissues are not exposed to the environment. Most closed (blunt) trauma is mild (75% to 90%) and causes mild concussion and classic cerebral concussion. Blunt trauma may result in both focal brain injuries and diffuse axonal injuries (DAI).

29.Define concussion. Know the different grades of concussion.

Concussion - different grades of concussion (p.588) Mild concussion • Grade I: Transient confusion and disorientation accompanied by amnesia (momentary); no loss of consciousness; symptoms resolve within 15 min. • Grade II: Transient confusion and retrograde amnesia that develops after 5-10 min (memory loss only of events occurring several minutes before injury); symptoms > 15 min. • Grade III: Any loss of consciousness (seconds or minutes); confusion and retrograde and anterograde amnesia remain from impact and persist several minutes. Classic cerebral concussion • Grade IV: any loss of consciousness (can last up to 6 hrs) accompanied by retrograde and anterograde amnesia.

16. Discuss disorders of the conjunctiva of the eye.

Conjunctiva of the eye - disorders(p.507 & 508) 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) o 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 o 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 o 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 o Is the result of any persistent conjunctivitis. The cause requires identification for effective treatment. Trachoma (chlamydial conjunctivitis) o 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.

30.Know coup and countrecoup brain injuries and how they happen.

Coup & Contrecoup Brain injury following blunt trauma (p. 583 & Fig 18-2 p. 584) Focal brain injury results from compression of the skull at the point of impact and rebound effects. May be a coup injury (directly below the point of impact) or contrecoup (on the pole opposite of site of impact). Objects striking FRONT of head usually produce only coup injuries (contusions and fractures), whereas objects striking the BACK of head usually result in coup and contrecoup b/c of irregularity of inner surface of the frontal bones; SIDE impact can result in either.

24.Define dyskinesia. Types? Characteristics?

Dyskinesia - Types & Characteristics (p.561-564) Unnatural movements that occur w/ variety of CNS dysfunctions which alter muscular innervation; neurotransmitter dopamine plays a role in motor function. Hyperkinesia: excessive movement (chorea, athetosis, ballism, hyperactivity, wandering, akathisia, Parkinsonian Tremor, asterixis, cerebellar, rubral, myoclonus) Paroxysmal dyskinesia: abnormal, involuntary movements that occur as spasms Tardive dyskinesia: involuntary movement of the face, trunk, and extremities. Usually occurs as a side effect of prolonged use of first or second generation antipsychotic drugs that cause denervation hypersensitivity, thereby mimicking the effect of excessive dopamine. The most common symptom of TD is rapid, repetitive, stereotypic movements, such as continual chewing with intermittent protrusions of the tongue, lip smacking, and facial grimacing. These are believed to be a form of excessive dopaminergic activity. Hypokinesia: a loss of voluntary movement despite preserved consciousness and normal peripheral nerve and muscle function. Types of Hypokinesia include akinesia, bradykinesia, and loss of associated movement. Akinesia: An absence, poverty or lack of control of associated and voluntary muscle movements. Is related to dysfunction of the extrapyramidal system, as in Parkinsonism. Pathogenesis is either a lack of dopamine or defect of postsynaptic dopamine receptors. Bradykinesia : slowness of voluntary movement. All voluntary movements become slow, labored, and deliberate. Difficulty in initiating, continuing, and performing synchronous and continuous tasks.

48.Define encephalocele, meningocele, spina bifida, myelomeningocele. Where is the defect located in each?

Encephalocele - definition and location of defect(p. 664) a herniation or protrusion of the brain and meninges through a defect in the skull, resulting in a sac like structure. Encephalocele occurs during the first weeks of pregnancy. When the defect contains only meninges, it is referred to as a cranial meningocele. Most encephaloceles occur in the occipital area, with the remainder found in the frontal, parietal, or nasopharyngeal regions Meningocele - definition and location of defect(p. 664) Type of spina bifida; saclike cyst of meninges filled with spinal fluid. It develops during the first four weeks of pregnancy when the neural tube fails to close completely. Meningocele is a structural anomaly of the posterior arch of the vertebra. The 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 cold. Meningoceles occur with equal frequency in the cervical, thoracic and lumbar spines. At birth the infant has a protruding sac on the back at level of the defect. Spina bifida - definition and location of defect(p. 664-666) When defects of the neural tube closure occur, such as meningocele or myelomenigocele, an accompanying vertebral defect allows the protrusion of the neural tube contents. This defect is called spina bifida (split spine). The cause of spina bifida is unknown. Periconceputal maternal folate deficiency and genetic alternations are commonly associated with the defect. It is also possible for the defect to occur without any visible exposure of meninges or neural tissue. This is referred to as spina bifida occulta. In spina bifida occulta the posterior vertebral laminae have failed to fuse. 80% of these vertebral defects are located in the lumbosacral regions, most commonly in the 5th lumbar vertebra and the first sacral vertebra Myelomeningocele - definition and location of defect(p. 665) Type pf spina bifida more common than meningocele and one of the most common developmental anomalies of the nervous system; cystic dilation of meninges and protuberance of various amounts of the spinal cord through the vertebral defect and assoc. w/ more severe complications than a meningocele. D/t changes in CSF flow, they are likely to be assoc. w/ a Chiari II malformation (downward placement of the cerebellum, brainstem, and fourth ventricle). The Chiari II compresses and stretches the posterior region of the cerebellum and brainstem downward through the foramen magnum ⇒ hydrocephalus, ↑ ICP from obstructed CSF flow, syringomyelia (causes cysts at multiple levels of spinal cord), and cognitive and motor deficits. *Location is evident at birth as a defect on the infant's back, 80% are located on in the lumbar and lumbosacral region, the last region to close up.

10.Know endogenous opioids.

Endogenous opioids (p.490) a family of morphine-like neuropeptides that inhibit transmission of pain impulses in the spinal cord, brain, and periphery. Play a role in various CNS, GI, immune system, and other organ system disorders. 4 types: Enkephalins—2 types: Met-enkephalin and Leu-enkephalin and their ratio is 4:1, respectively. They are found 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.

12.What is the relationship between epinephrine and body temperature?

Epinephrine's relationship to body temp (P.496) 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. Pathogenesis of Fever (p.498) -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.

6. What is the gate control theory of pain?

Gate control theory of pain (p.485) Pain transmission is modulated by a balance of impulses transmitted from large, myelinated A-Delta (responsible for well-localized, sharp pain sensations) and small, unmyelinated C fibers (transmit diffuse burning or aching sensations). These fibers terminate on inhibitory neurons in the substantia gelatinosa (SG) (lamina in the dorsal horn of the spinal cord). Cells in the SG function as a "gate", regulating transmission of impulse to the CNS. Stimulation of non-nociceptive larger A-Beta fibers such as touch, vibration or thermal stimuli, cause the cells in the SG to "close the pain gate" which diminishes pain perception. This is why rubbing a painful area may alleviate some of the discomfort. The CNS, through efferent pathways may also close, partially close, or open the "gate".

45.How Does ECT (electroconvulsive therapy) treat depression?

How ECT treats depression(p. 652) ECT is used when individuals fail to respond to antidepressants or when they are severely depressed, pregnant, suicidal, or psychotic. ECT effectively alleviated depressive symptoms in 50-80% of people. The mechanism of action in ECT is unclear, but the procedure is known to produce alterations in monoamine systems. Electrodes are implanted into the subcallosal cingulate gyrus (SCG) and attached to an implanted pulse generator through SQ extension wires. The SCG is targeted because abnormal SCG brain activity, a suggested pathophysiologic cause of major depression, is reversed by effective antidepressant treatment.

46.Define generalized anxiety disorder. What is the underlying defect? Know characteristics

Generalized Anxiety Disorder - underlying defect & characteristics(p. 655) Excessive and persistent worries are the hallmarks in GAD. Worries about life events, marital relationships, job performance, health, money, or social status. The prevalence rate is 4.1-6.6% and higher rate in women. GAD emerges in early twenties but also can occur in childhood. There are 6 major symptoms: restlessness, muscle tension, irritability, easily fatigued, difficulty concentrating, and difficulty sleeping. They suffer from depression and panic attacks. GAD tends to be chronic, but may lessen with age. Substance abuse is a frequent complication (drug and alcohol to self-medicate). This is caused by abnormalities in norepinephrine and serotonin systems that include: reduction in a2-adrenergic receptor binding, decreased serotonin levels in CSF, a reduction in platelet binding paroxetine, an SSRI. Also a reduction of BZ binding in left temporal hemisphere. GAD is diagnosed when a person spends at least 6 months worry excessively and engages in at least 3 of the 6 major symptoms. 5-HT/norepinephrine reuptake inhibitors, such as venlafaxine or the SSRIs paroxetine and escitalopram, have become first-line therapeutics for management of GAD.

14.Know heat exhaustion and heat stroke?

Heat exhaustion & heat stroke (p.500) Heat Exhaustion—The result of prolonged 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.

13.Know mechanisms of heat production and heat loss.

Heat production and heat loss - mechanisms (p.496-497) 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 non-shivering 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—refers to heat loss by direct molecule-to-molecule transfer 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 ↓ heat production, muscle tone may be moderately ↓ and voluntary muscle activity curtailed 6) Evaporation—evaporation of body water from the surface of the skin and the linings of the mucous membranes is a major source of heat reduction. 7) Increased pulmonary ventilation—exchanging air with the environment through the 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.

41.Define and describe the pathophysiology, clinical manifestations and etiology of Huntington disease.

Huntington Disease - Pathophysiology, Clinical Manifestations & Etiology(p. 562-564) Pathophysiology The major pathologic feature of HD is severe degeneration of the basal ganglia and the frontal cerebral cortex. Degeneration of the basal ganglia and the substantia nigra exhibit a depletion of neurons that secrete GABA (an inhibitory neurotransmitter). GABA depletion leads to an excess of dopaminergic activity that causes hypotonia and hyperkinesia (involuntary, fragmentary movements). Clinical Manifestations Abnormal movement and progressive dysfunction of intellectual processes (dementia) and emotional lability. Chorea (involuntary, quick movements of the feet or hands comparable to dancing) is the most common type of abnormal movement affecting individuals with HD. It begins in the face and arms, eventually affecting the entire body. Symptoms of frontal lobe dysfunction include attention deficits, short term memory loss, reduced capacity to plan, organize, and sequence, as well as bradyphrenia (slow thinking); and apathy. Etiology HD (Chorea) is a rare, hereditary (autosomal dominant)-degenerative disorder diffusely involving the basal ganglia and cerebral cortex, commonly manifests between 25-45 years of age, and occurs in all races. The abnormality is manifested on the short arm of chromosome 4. Treatment No known treatment is effective in halting the degenerative process in HD. The chorea can be treated with dopamine receptor-blocking or depleting agents, and medical and non- medical care for depression and aggressive behavior may be required.

25.Know the stages of intracranial hypertension.

Intracranial hypertension (stages and compensatory mechanisms for ↑ ICP) (p. 555-557) *NORMAL INTRACRANIAL PRESSURE (ICP) = 5-15mmHg OR 60-180 mm H₂O. The RED font indicates the compensatory mechanisms for ↑ ICP. Stage 1: Cerebral blood volume is altered which causes intracranial hypertension. Vasoconstriction and external compression of the venous system occur in an attempt to further decrease the intracranial pressure. Thus, the ICP may not change due to compensatory mechanisms {CSF is reduced through increased reabsorption. Blood volume is reduced by compression of intracranial veins.} 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. Stage 2: There is continued expansion of intracranial content; the resulting increase in ICP may exceed the brain's compensatory capacity to adjust. 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 usually subtle and transient, including episodes of confusion, restlessness, drowsiness, and slight pupillary and breathing changes. Stage 3: The ICP begins to approach arterial pressure, the brain tissues begin to experience hypoxia and hypercapnia, and the individuals condition rapidly deteriorates. Clinical manifestations include decreasing levels of arousal or central neurogenic hyperventilation, widened pulse pressure, bradycardia, and pupils that 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 its blood supply. Small hemorrhages often develop in the involved brain tissue. Obstructive hydrocephalus may develop. The herniation process markedly and rapidly increases intracranial pressure. Mean systolic arterial pressure soon equals ICP and cerebral blood flow ceases at this point. The types of herniation syndromes are outlined in box 17-4.

19.Discuss the types of mid-brain dysfunction and its physical symptoms.

Midbrain dysfunction types and physical symptoms (p. 459, 558, & 565) The midbrain is part of the brainstem and is composed of three structures: 1.) corpora quadrigemina (composed of the superior and inferior colliculi), 2.) tegmentum (containing the red nucleus and substantia nigra) 3.) basis pedunculi. The superior colliculi are involved with voluntary and involuntary visual motor movement. Inferior colliculi involve movement affecting the auditory system (moving the head to improve sound). The red nucleus is a major motor output center that is influenced by the cerebellum. Substantia nigra: Most inferior part of the basal ganglia (corgus striatum, globus palidus, subthalamic nucleus, and sustantia nigra); synthesizes dopamine which is a neurotransmitter and precursor of norepinephrine. Its dysfunction is associated with Parkinson Disease and drug addiction. Parkinson disease is a complex motor disorder accompanied by systemic nonmotor and neurologic symptoms. The main disease feature is degeneration of the basal ganglia which include the substantia nigra. Hallmark feature of PD is loss of dopaminergic pigmented neurons in the substantia nigra pars compacta with dopaminergic deficiency in the putamen portion of the striatum. Degeneration of the dopaminergic nigrostriatal pathway to the basal ganglia results in underactivity of the direct motor pathway and over activity of the indirect motor loop. This results in inhibition of the motor cortex manifested with bradykinesia and rigidity. Classic symptoms are bradykinesia (poverty of associated and voluntary movements), tremor at rest, rigidity (muscle stiffness), hypoakinesia (poverty of movement), and postural abnormalities. Other notable structures of this region are the nuclei and tracts of the third and fourth cranial nerves. The cerebral aqueduct (aqueduct of Sylvius), which carries CSF, also traverses this structure. The obstruction of this aqueduct is often the cause of hydrocephalus. Hydrocephalus occurs because of interference with CSF flow caused by increased fluid production, obstruction within the ventricular system, or defective reabsorption of the fluid. Symptoms include the person deteriorating rapidly into a deep coma or it might develop slowly overtime. An unsteady, broad gate with a history of falling is common. Apathy, inattentiveness, urinary incontinence, and indifference to self, family, and the environment.

39.Define and describe the pathophysiology, clinical manifestations and etiology of Mysthenia Gravis

Myasthenia Gravis - Pathophysiology, Clinical Manifestations, & Etiology (p. 624-626) Pathophysiology Myasthenia gravis results from a defect in nerve impulse transmission at the neuromuscular junction. The main defect is the formation of autoantibodies (an IgG antibody) against receptors at the ACh binding site on the postsynaptic membrane. The autoantibodies block the AChR or cause complement- mediated loss of AChRs from the neuromuscular junction. The cause of this auto sensitization is not known. The destruction of receptor sites causes diminished transmission of the nerve impulses across the neuromuscular junction. Muscle depolarization is incomplete or not achieved. Clinical Manifestations Myasthenia gravis typically has an insidious onset. clinical manifestations may first appear during pregnancy, during postpartum period, or in conjunction with the administration of certain anesthetic agents. The foremost complaint is muscular fatigue and progressive weakness. The individual often complains of fatigue after exercise and has a recent history of reoccurring upper respiratory tract infections. The muscles of the eyes, face, mouth, throat, and neck usually are affected first. The extra occular eye muscles and the levator muscles are most affected. Manifestations include diplopia, ptosis, and ocular palsies. The muscles of facial expression mastication, swallowing, and speech are the next most involved. The results are facial droop and an expressionless face; difficulty chewing and swallowing. The muscles of the neck, shoulder girdle, and hip flexors are affected less frequently. When involved the person experiences fatigue requiring periods of rest, weakness of the arms and legs that improves with rest, and difficulty in maintaining head position. The respiratory muscles of the diaphragm and the chest wall become weak, and ventilation is impaired. Impairment n deep breathing and coughing predisposes the individual to atelectasis and congestion. In the advance stage of the disease, all the muscles are weak. Etiology The etiology of myasthenia gravis is unknown. Some persons have genetic susceptibility related to variants in AChR genes, as well as the major histocompatibility genes. diagnosis: The diagnosis of MG is made on the basis of a response to endeophonium chloride (Tensilon), results of repetitive single-fiber EMG, and detection of AchR and MuSK antibodies. Treatment Treatment is individualized. Anticholinesterase drugs, corticosteroids, immunosuppressant drugs, azithroprine, and cyclosporine are used to treat MG. Plasmapheresis (plasma is separated from cells and is replaced) may be life-saving during a crisis.

52.What nerves are capable of regeneration?

Nerves capable of regeneration(p. 450-451) Myelinated axons ONLY in the PNS. When an axon is severed wallerian degeneration occurs in the portion of the axon distal to the cut: 1) a characteristic swelling appears 2) the neurofilaments hypertrophy 3) the myelin sheath shrinks and disintegrates 4) this axon portion degenerates and disappears. The myelin sheaths reform into Schwann cells that line up in a column between the cut and the effector organ. At the proximal end of the injured axon, similar changes occur but only as far back as the next node of Ranvier. The cell body responds to trauma by swelling and then dispersing the Nissl substance (chromatolysis). During the repair process the cell increases in metabolic activity, protein synthesis, and mitochondrial activity. This process is limited to myelinated fibers and generally doesn't occur outside of the PNS. The regeneration of axonal constituents in the CNS is limited by increased scar formation and the different nature of myelin formation by the oligodendrocyte. Nerve regeneration depends on many factors, such as location of injury, type of injury, the inflammatory responses, and the process of scarring. The closer the cell body of the nerve, the greater the chances that the nerve cell will die and not regenerate. A crushing injury allows recovery more fully than a cut. Crushed nerves sometimes recover whereas, cut nerves often form connective tissue scars that block or slow regenerating axonal branches.

27.Know the most critical index of nervous system dysfunction/function.

Nervous system function/dysfunction - most critical index(p.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. Highest level of Consciousness is alert, oriented to self, others, place and time (implies full use of cognitive capacities). Levels of altered consciousness include: confusion, disorientation, lethargy, obtundation, stupor, coma, light coma, coma, and deep coma.

51. Know pathophysiology, clinical manifestations and etiology of PKU.

PKU - Pathophysiology, Clinical manifestations and Etiology(p. 673-674) Etiology—PKU is an autosomal recessive, inborn error in the metabolism of amino acids. Pathophysiology - Characterized by mutations of the phenylalanine hydroxylase (PAH) gene. Most natural food proteins contain about 15% phenylalanine. Loss of PAH results in phenylalanine hydroxylase deficiency and the inability of the body to convert the amino acid phenylalanine to tyrosine. It is the accumulation of phenylalanine that causes damage to the CNS. Clinical Manifestations - When a baby born with PKU and begins a regular diet high in phenylalanine, buildup occurs, brain growth slows, and the child exhibits developmental delays or intellectual disability, concomitant with jerking movements, seizures, skin rashes and attention problems. Children with PKU have a phenotype that includes blonde hair, blue eyes and fair skin- due to the biosynthesis of melanin. Individuals with PKU need to be screened for response to BH4, which decreases blood phenylalanine levels when given an oral supplement. Treatment - restriction of phenylalanine in the diet and supplementation with other essential amino acids. Treatment must be continued for life and strict adherence for pregnant women.

7. Know the type of nerve fibers that transmit pain impulses.

Pain impulses - nerve fibers that transmit them (p.486) Nociceptors (primary order neurons) are free nerve endings in the afferent peripheral nervous system that selectively respond to different chemical, mechanical, and thermal stimuli. Nociceptors are categorized according to the stimulus to which they respond and by the properties of the axons associated with them. A-delta fibers: lightly myelinated, medium-sized fibers that are stimulated by severe mechanical deformation and/or by extremes of temperature. These fibers rapidly transmit sharp, well-localized "fast" pain sensations and are responsible for casing reflex withdrawal of the affected body part from the stimulus. C-fibers: polymodal; stimulated by mechanical, thermal, and chemical nociceptors. They slowly transmit dull, aching, or burning sensations that are poorly localized and longer lasting. A-beta fibers: large myelinated fibers that transmit touch and vibration sensations. They do not normally transmit pain but do play a role in pain modulation.

8. Where in the CNS does pain perception occur?

Pain perception - where in the CNS it occurs (p.487, and look at Fig 16-4 p.489) Pain perception is the conscious awareness of pain. Three systems interact to produce the perception of pain and individual responses to pain. I. Sensory-discriminative system—mediated by the somatosensory cortex and is responsible for identifying the presence, character, location and intensity of pain II. Affective-motivational system—determines an individual's conditioned avoidance behaviors and emotional responses to pain. It is mediated through the reticular formation, limbic system, and brainstem with projections to the prefrontal cortex. III. Cognitive-evaluative system—overlies the individual's learned behavior concerning the experience of pain and can modulate perception of pain. Mediated through the cerebral cortex.

47.Define panic disorder. What are the complications?

Panic Disorder - Complications(p. 654) Panic disorder consists of multiple disabling panic attacks and is characterized by intense autonomic arousal involving wide variety of symptoms: light headedness, rapid heart rate, difficulty breathing, chest discomfort, generalized sweating, general weakness, trembling, abdominal distress, chills or hot flashes. Between panic attacks, individuals worries about future panic attacks and fear of losing control or dying. Symptoms occur spontaneous and vary in length from several minutes to hours. A notable complication from panic disorder is the development of agoraphobia or phobic avoidance of places or situations where escape or help is not readily available. They avoid being away from home, standing in lines, crowds, traveling in a train, plane, or automobile. Severe agoraphobia individuals become housebound.

40.Define and describe the pathophysiology, clinical manifestations and etiology of Parkinsons disease.

Parkinson Disease - Pathophysiology, Clinical Manifestations, & Etiology(p. 564-568) Pathophysiology The hallmark pathologic features of Parkinson disease are loss of dopaminergic pigmented neurons in the substantia nigra (SN) pars compacta with dopaminergic deficiency in the putamen portion of the striatum (the striatum includes the putamen and caudate nucleus). Dopamine loss in other brain areas including the brainstem, thalamus, and cortex also occurs. Degeneration of the dopaminergic nigrostriatal pathway to the basil ganglia results in underactivity of the direct motor pathway (normally facilitates movement) and over activity also influences the limbic system accounting for emotional signs and symptoms. Neuronal loss within the cerebral cortex is found in one half of individuals with PD. Manifestations Onset of symptoms is insidious and symptoms appear after 70% to 80% loss of pigmented nifral neurons and loss of 60% to 90% of striatal dopamine. The classic motor manifestations of PD are bradykinesia, tremor at rest (resting tremor), rigidity (muscle stiffness), hypoakinesia (poverty of movement), and postural abnormalities. These manifestations may develop alone or in combinations, but as the disease progresses, all four are usually present to at least some degree, there is no true paralysis. Etiology Etiologic classifications of parkinsonism includes primary parkinsonism and secondary parkinsonism (BOX 17-5 on p. 565 gives all of the causes of each). The onset of PD occurs after 40 years of age, with mean onset of 60 years of age. Equal incidence occurs in both sexes. PD is one of the most prevalent of the primary CNS disorders and a leading cause of neurologic disability in individuals older than 60 years. Evaluation & Treatment The diagnosis of PD is made on the basis of the four cardinal symptoms: resting tremor, cogwheel rigidity, akinesia, and postural instability. The aim of treatment is to restore striatal dopamine levels using oral drugs such as levodopa, a precursor of dopamine.

43.What is schizophrenia? What part of the brain is associated with the S/S of this disorder?

Schizophrenia - definition, part of brain associated, and prenatal and perinatal contributing factors(p. 642-647) Schizophrenia is a serious psychiatric illness that strikes 1% of the population; equally prevalent in males and females, emerging in young adults during late teens and early twenties. The term was coined by Eugen Bleuler in 1911 to describe a collection of illnesses characterized by thought disorders, reflecting a break in reality or splitting of the cognitive from emotional side of personality. (+) symptoms include auditory hallucinations, paranoid delusions, formal thought disorder, and bizarre behavior. (-) symptoms are flat affect, alogia (lack of speech), anhedonia (absence of pleasure), attention deficits and apathy. Prenatal & Perinatal Contributors & Parts of brain associated Early development may involve issues from environmental factors (viral infection during pregnancy, prenatal nutritional deficiencies, prenatal birth complications, and perinatal complications such as birth defects and neonatal hypoxia) which may interfere with genetic programming of neural development leading to alterations in brain structure and function. There is a strong genetic component. Structural brain abnormalities present on imaging. Enlargement of cerebroventricles and widening of fissures and sulci in frontal cortex. Reduction in the volume of the thalamus, disrupting communication among cortical brain regions, and the TEMPORAL LOBE, which may be RESPONSIBLE FOR MANIFESTATIONS OF POSITIVE SYMPTOMS. Frontal lobe has a progressive loss of volume and worsening of negative symptoms even with use of antidepressants. Functional alterations in the dorsolateral prefrontal cortex, (reduced blood flow and metabolism) compromise abilities to engage in goal-directed and cognitive problem - solving behavior. Abnormalities of Schizoid brains is in the neurochemicals dopamine and excitatory amino acid neurotransmission. Structural brain abnormalities present on imaging include enlargement of lateral and third ventricles and widening of the frontocortical fissures and sulci. With cerebral ventricular changes, the patient is likely to have cognitive impairments and negative symptoms. They also respond poorly to treatment. With temporal lobe alterations, patient has positive symptoms. With dorsal prefrontal cortex changes, negative symptoms are present. Especially with dorsolateral prefrontal cortex (DLPFC), initiation and maintenance of goal oriented activities and solving cognitive problems in relation to working memory is impaired

22.Define seizure and status epilepticus. What is the medical significance? Know benign febrile seizures.

Seizure (p.550) sudden, transient disruption in brain electrical function caused by abnormal excessive hypersynchronous discharges of cortical neurons. Benign febrile seizure(p.679) Febrile seizure is associated w/ fever in absence of cranial nerve system infection; Simple febrile seizures are benign, occur in 2-5% children, but are most common childhood seizure. Pathogenesis is unknown; a familial incidence indicates a genetic predisposition. Contributing factors are age, degree and rate of temperature elevation, and nature of the particular fever-inducing illness. Status epilepticus (p.553) in adults is a state of continuous seizures lasting more than 5 minutes, or rapidly recurring seizures before the person has fully regained consciousness from the preceding seizure, or a single seizure lasting more than 30 minutes. SE can arise from abnormal persistence of excessive excitation or ineffective recruitment of inhibition. The person is still in a postictal state (a state that follows an epileptic seizure and returns to baseline) when the next seizure begins. SE most often results from abrupt discontinuation of antiseizure medications 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, other brain damage, and even death are serious threats. Aspiration also is a great risk

15.Define the different stages of sleep.

Stages of sleep(p.502-504) 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: o awake: wakefulness with eyes closed and predominated by alpha waves (8-25 Hz) o N1 - light sleep with alpha waves (6-8 Hz) interspersed with low frequency theta waves; slow eye movements (3-8% of sleep time) o N2 - further slowing of the EEG (4-7 Hz) with the presence of sleep spindles and slow eye movements (45-55% of sleep time) o 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. A small group of hypothalamic nerve cells, the suprachiasmatic nucleus, controls the timing of the sleep wake cycles.

33.Know diagnostic criteria for vegetative state and brain death.

Vegetative state -diagnostic criteria for Persistent Vegetative State (PSV) (p. 534) A wakeful unconscious state. Diagnostic Criteria: 1) periods of eye opening (spontaneous or following stimulation 2) the potential for subcortical responses to external stimuli, including generalized physiologic responses to pain, such as posturing, tachycardia, and diaphoresis, and subcortical motor responses, such as grasp reflex 3) return of so-called vegetative (autonomic) functions, including sleep-wake cycles and normalization of respiratory and digestive system functions 4) occasional roving eye movements without concomitant visual tracking ability. (The person's eyes open spontaneously or following stimulation, or both.) There may be random hand 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 - diagnostic criteria(p. 533-534) An isoelectric, or flat, electroencephalogram (EEG) (electrocerebral silence) 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 and usually means that the brain is already dead. Brain death in children has same criteria as adults but a longer observation period. Summary of criteria: 1. Completion of all appropriate and therapeutic procedures w/ no possibility of brain function recovery. 2. Unresponsive coma (absence of motor and reflex movements) 3. no spontaneous respiration (apnea)—a PaCO2 that rises above 60 mmHg without breathing efforts, providing evidence of a nonfunctioning respiratory center (apnea challenge) 4. No brainstem function (ocular responses to head turning or caloric stimulation; dilated, fixed pupils; no gag or corneal reflex) 5. Isoelectric (flat) EEG (electrocerebral silence) 6. Persistence of these signs for 30 mins- 1hour and for 6 hours after onset of coma and apnea

42.Prenatal and perinatal factors may result in what psychiatric condition?

pg 642 Some of the prenatal and perinatal factors that may result in schizophrenia are: exposure to prenatal infection, prenatal nutritional deficiencies, perinatal complications (such as birth defects and neonatal hypoxia).