NURS 5315 Patho Module 7 Study Guide DOWNLOAD for an A, Exams of Nursing

Download NURS 5315 Patho Module 7 Study Guide DOWNLOAD for an A and more Exams Nursing in PDF only on Docsity! 1 N5315 Advanced Pathophysiology Neurologic System Module 7 Examine the anatomy and physiology of the Central Nervous System. 1. Discuss the anatomy and physiology of the brain and brain stem. a. Explain the function of the twelve cranial nerves I – Olfactory (Smell) Function: Sensory, carries impulses for sense and smell Sign of Dysfunction: Loss or disturbance in the sense of smell. II – Optic (Sight) Function: Sensory, carries impulses for vision Sign of Dysfunction: decreased visual acuity and contrast sensitivity, impaired color vision, and an afferent pupillary defect. (blindness) III – Oculomotor Function: Contains motor fibers to interior oblique and to superior, inferior, ad medial rectus extraocular muscles that direct eye ball; levator muscles of eyelid; smooth muscles of iris and ciliary body; and proprioception (sensory) to brain from extraocular muscles Sign of Dysfunction: Drooping of the eyelid, eyeball moves outward, dilation of the pupil, double vision. IV – Trochlear Function: Propioceptor and motor fibers for superior oblique muscle of eye (extraocular muscles) Sign of Dysfunction: Rotation of eyeball upward and outward, double vision V Trigeminal (facial muscles including chewing, facial sensation) This is the largest cranial nerve Function: Both motor and sensory for face; conducts sensory impulses from mouth, nose, surface of eye, and dura mater; also contains motor fibers that stimulate chewing muscles Sign of Dysfunction: Sensory root – Pain or loss of sensation in the face, forehead, temple and eyes. Motor root – affecting the jaw, trouble chewing VI Abducens (moves eyeballs) Function: Moves the eyeballs outwards by sending nerve impulses to the lateral rectus muscles Sign of Dysfunction: Deviation of the eyes outward; double vision 2 VII Facial (taste, tears, saliva and facial expressions) Function: Mixed: 1. Supplies motor fibers to muscles of facial expression and to the lacrimal and salivary glands. 2. Carries sensory fibers from taste buds of anterior part of tongue Sign of Dysfunction: Paralysis of all the muscles in one side of the face, inability to wrinkle the forehead, close the eye, whistle, deviation of the mouth. Bell’s Palsy VIII Vestibulocochlear (acoustic) auditory Function: Purely sensory; vestibular branch transmits impulses for sense of equilibrium, cochlear branch transmits impulses for sense of hearing Sign of Dysfunction: Deafness or ringing in the ears, dizziness, nausea and vomiting IX Glossopharyngeal (swallowing, saliva, taste) Function: Mixed: 1. Motor fibers serve pharynx and salivary glands. 2. Sensory fibers carry impulses from, pharynx, posterior tongue, and pressure receptor of carotid artery (blood pressure) Sign of Dysfunction: Disturbance of taste; Difficulty in swallowing X Vagus (control of PNS: smooth muscles of GI tract) Function: Sensory and motor impulses for pharynx; a large part of this nerve is parasympathetic motor fibers, which supply smooth muscles of abdominal organs Sign of Dysfunction: Hoarseness and difficulty swallowing and talking. This nerve also regulates the heart, blood vessels and digestion resulting in irregular heartbeat and lowered blood pressure. It regulates the stomach telling it to move food through the digestive system, thus damage can result in decreased digestion and thus nausea, bloating and vomiting. XI Spinal accessory (moving of head and shoulders, swallowing) Function: Provides sensory and motor fibers for sternocleidomastoid and trapezius muscles (movement of head and shoulders) and muscles of soft palate, pharynx, and larynx (swallowing) Sign of Dysfunction: Dropping of the shoulder; inability to rotate the head away from affected area. XII Hypoglossal (tongue muscles, speech and swallowing) Function: Carries motor fibers to muscles of tongue and sensory impulses from tongue to brain. Sign of Dysfunction: Paralysis of one side of the tongue; deviation of tongue toward paralyzed side; thick speech. 5 Location: Brain Stem (midbrain, medulla oblongata, and pons) Located at the base of the brain Function: Medulla: regulate breathing and blood pressure, swallowing, coughing and vomiting reflexte Pons: balance and maintainence of posture and regulation of breathing. Relays information from cerebral hemispheres to teh cerebellum Midbrain: control of eye movements and visual systems Sign of Injury/Lesion/Disorder: Loss of function- breathing, regulate BP, protective reflexes for airway Location: Reticular Formation and Reticular Activating System Brainstem: A collection of nuclei within the brainstem p454 (reticular formation in conjuction with the cerebral cortex is referred to as the Reticular Activating System) Function: maintaining wakefulness Maintains vital reflexes ( cardiovascular function and respiration Sign of Injury/Lesion/Disorder: Alterations in consciousness Location: Limbic System Forebrain: Composed of Papez circuit – (amygdala, parahippocampal gyrus, hippocampus, fornix, mammillary body of the hypothalamus, thalamus, cingulate gyrus), septal area, habenula, nucleus accumbens, other portions of the hypothalamus, related autonomic nuclei. Function: Consolidation of memory, Extension of olfactory system. Primitive behavioral responses, visceral reaction to emotion, feeding behaviors, biologic rhythms, and sense of smell Basic emotion area – fear, pleasure, anger, and drives (hunger, sex, dominance, care of offspring). Primitive behavioral responses, visceral reaction to emotion, feeding behaviors, biologic rhythms, sense of smell. A major function is consolidation of memory through a reverberating circuit. Sign of Injury/Lesion/Disorder: 6 c. Identify which area of the brain is impacted by a disorder based on the clinical manifestation. -Agnosia- failure to detect a pattern, failure to recognize the form and nature of objects when holding them by feel but can name them by sight. Dysfunction is in the primary sensory area or the interpretive areas of the cerebral cortex (temporo-occipital area). -Dysphasia- impairment of comprehension or production of language) semantic processing). Either comprehension or use of symbols, in either written or verbal language, is disturbed or lost. Aphasia is loss of comprehension or production of language. Usually associated with CVA involving the middle cerebral artery or one of its branches. Can be from vascular, traumatic or degenerative processes. Dysphasia dysfunction in the L cerebral hemisphere, most common in the frontotemporal region around the insular cortex, deep in the lateral sulcus. Expressive dysphasias- primary expressive deficits but has verbal comprehension. Transcortical dysphasia – speech is fluent but with striking paraphrases, and the person cannot read, write and comprehension is impaired. Caused by prolonged hypotension, carbon monoxide poisoning. Affects the border zone (watershed area) of anterior, middle, and posterior cerebral arteries (blood supply is marginal in this region) d. Discuss the function and location of the Wernicke and Broca’s areas of the cerebrum and describe a sign which would manifest as a result of a lesion, injury or defect in each area. Wernicke Area Location: Forebrain: Superior temporal gyrus Function: Reception and interpretation of speech Sensory speech area Sign of Injury: Dysfunction results in receptive aphasia or dysphagia - patients cannot understand the verbal language at all. Broca’s Area Location: Forebrain: Left hemisphere; inferior edge of the premotor area Function: Responsible of motor aspects of speech Sign of Injury: Dysfunction usually results from stroke; inability to or difficulty in forming words; (expressive aphasia or dysphasia) 7 e. Explain the difference between supratentorial and infratentorial. Supratentorial Definition: There are four types of supratentorial herniations. II An uncal herniation occurs when a portion of the gyri of the cerebrum moves through the tentorial notch and compresses the third cranial nerve and the mesencephalon. Manifestations include decreased LOC, dilated ipsilateral pupil first, then the contralateral pupil, decorticate or decerebrate posturing, and Cheyne stokes respirations. III A central herniation occurs when the diencephalon is forced down and through the tentorial notch. These individuals lose consciousness quickly, develop apnea, initially have small reactive pupils and later they dilate. Decorticate posturing or decerebrate posturing becomes evident. IV A cingulate gyrus herniation is characterized by the movement of the cingulate gyrus under the falx cerebri. Instead of moving down, it moves laterally. This herniation is labeled number 3 in the picture. Transcalvarial (trans.kal.ver.al) herniation is characterized by brain tissue which moves through an opening in the skull. The opening may be a result of a skull fracture or a surgical opening. Infratentorial Definition: The main infratentorial herniation is the cerebellar tonsillar herniation, the most common type of brain herniation. It is characterized by the downward movement of the cerebellum through the foramen magnum. Clinical manifestations include a stiff neck, a decreased LOC, respiratory abnormalities, and pulse variations. f. Discuss the cerebral artery anatomy and identify which artery provides blood to which part of the brain. Internal carotid arteries- anteriorly, supply a proportionately greater amount of flow. Originate- common carotid artery, enter cranium through base of skull, pass through cavernous sinus and divide into anterior and middle cerebral arteries- Anterior serves the basal ganglia, corpus callosum, medial surface of the cerebral hemispheres, the superior surface of the frontal and parietal lobes. Occlusion here would cause hemiplegia on the contralateral side of the body, greater in the lower than upper extremities. Middle serves the frontal, parietal, and temporal lobes. Occlusion here would cause aphasia in the dominant hemisphere (usually the left), contralateral paralysis and loss of sensation. Vertebral arteries- posteriorly, originate as branches off the subclavian arteries, pass through transverse foramina of cervical vertebrae, enter cranium through foramen magnum, join at junction of the pons and medulla to form basilar artery. Basilar artery divides at midbrain to form paired posterior cerebral arteries. Posterior serves the occipital lobe and occlusion here would cause visual changes, contralateral to the occlusion (cross-over of the optic nerve). Basilar serves the pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, and the ocular cranial nerve. Occlusion here results in quadriplegia, loss of voluntary facial, mouth, and tongue movements. Person’s consciousness remains intact but they are “locked in”. 10 Beta 2 Location: Lungs Heart (coronary), eye, skeletal muscle, kidney, systemic veins, bronchial glands, stomach motility, intestinal motility & tone, bladder, fat cells Function: Smooth muscle relaxation S- dilation P- opposite N/M Clinical Implications: bronchodilates 4. Describe the structural, cellular and cerebrovascular and function age related changes which affect the nervous system. Age-related effects Structural change Decreased brain weight and size, particularly frontal regions Fibrosis and thickening of the meninges Narrowing of gyri and widening of sulci Increase in size of ventricles Age-related effects Cellular Change Decreased amount of myelin, Lipofuscin deposition (a pigment resulting from cellular autodigestion) Decreased number of dendritic processes and synaptic connections Formation of intracellular neurofibrillary tangles; significant accumulation in cortex associated with Alzheimer dementia Imbalance in the amount and distribution of neurotransmitters Decrease in the number of neurons, not consistently related to changes in mental function Age-related effects Cerebrovascular change Arterial atherosclerosis (may cause infarcts and scars) Increased permeability of the blood-brain barrier Decreased vascular density 11 Functional change Age-related effects Decreased tendon reflexes Skeletal muscle atrophy Progressive deficit in taste and smell Decreased vibratory sense Decrease in accommodation and color vision Decrease in neuromuscular control with change in gait and posture Sleep disturbances Memory impairments Cognitive alterations associated with chronic disease Functional changes and nervous system aging have significant individual variation 5. Explain the embryonic development of the CNS and the brain development of the infant and child. · Embryonic CNS Development: § CNS develops from a dorsal thickening of the ectoderm (neural plate) around the 3rd week of gestation and unfolds to form a neural groove and neural folds. § Neural groove deepens during the 4th week of gestation, its folds develop laterally, and closes dorsally to form the neural tube which ultimately becomes the CNS § Neural tube closes first in the cervical region then “zippers” in two directions – cranially to caudally § Some neroectodermal cells separate from the neural tube but, remain between the tube and surface ectoderm = neural crest § Neural crest develops into the cranial and spinal ganglia = PNS § Blood vessels, microglial cells, dural and arachnoid layers of the meninges, the capsule of some peripheral sensory nerve endings, and peripheral nerve coverings arise from the mesoderm (somite) § The cranial end of the neural tube forms the brain and the remainder develops into the spinal cord. § The lumen of the neural tube becomes the ventricles of the brain and the central canal of the spinal cord § The alar plate (region posterior to the sulcus) differentiates into the sensory nuclei of the spinal cord. § Occurs in six stages: 1. Dorsal (posterior) induction 2. Ventral (anterior) induction 3. Proliferation 4. Migration 5. Organization 6. Myelination 12 · Embryonic Brain Development: § Forms from the cranial end of the neural tube § Ventricles are formed from the lumen of the neural tube § The basal plate forms the gray matter which differentiates into the nuclie of the lower motor neurons. · Infant & Child Brain Development: § At birth the bones in the skull are separated at the suture lines creating the anterior and posterior fontanels “soft spots” o The anterior fontanel is diamond shape and normally closes by 18 months of age o The posterior fontanel is triangular shaped and may be open until 2-3 months of age o The sutures are not closed allows for increases in head circumference as part of normal growth after birth until 5 – 8 yrs after birth o The head is the fastest growing body part during infancy. § Basically, all of the neurons an individual will ever have are present at birth, skill development is dependent on the cells making correct connections with other cells and on myelination of the axons making those connections. This leads to brain and skull growth § Increased intracranial pressure may result in an increased head circumference (HC) in excess of that expected with normal growth. § Head growth is monitored closely during the first 5 years of life by measuring HC and comparing the results on standardized growth charts. § Connections between brain circuits, myelination of those connections, and dendritic development are most significant after birth. Examine the pathologic basis of adult and pediatric disorders which affect the nervous system. Disorders of Speech 6. Describe the types of dysphasia, their clinical manifestations, the location of the dysfunction, the etiology and the implications for clinical practice. Expressive Dysphasia Clinical Manifestations – Unable to find the words to speak or write Location of Dysfunction – Broca’s area of the frontal lob Etiology - Occlusion of branches of MCA, trauma, tumor, infection, abscess Clinical Implications – Verbal comprehension is usually intact. They can follow commands. They can understand you but cannot express what they would like to. 15 Risk Factors Alzheimer’s Disease Age, family history, DM, midlife HTN, hyperlipidemia, midlife obesity, smoking, depression, cognitive inactivity, low educational attainment, female gender, estrogen deficiency at the time of menopause, physical inactivity, head trauma, neuroinflammation and oxidative stress. Linked to an autosomal dominant inheritance pattern Etiology unknown some cases linked to autosomal dominant inheritance pattern Early onset 10% (familial): (Genes: amyloid precursor protein (APP) on chromosome 21, presenilin 1 (PSEN1) on chromosome 14, and PSEN2 on chromosome 1) Pathophysiology Most common form of dementia. Progressive, degenerative disease of the brain that results in impaired memory, confusion, visual spatial disorientation, inability to calculate and impaired judgment. Typically onset is usually late middle life and death occurs in five-ten years after diagnosis. Accumulation of amyloid in the brain which causes neurofibrillary tangles which is the distortion and twisting of neurons. Senile plaques are then formed. This leads to the disruption of nerve impulse transmission, neuron death, loss of function and death. Clinical Manifestations Hallucinations. Leads to loss of independence, leaving the individual requiring assistance with bathing, eating, dressing and toileting. General Disorders of the Nervous System 8. Differentiate between the etiology, clinical manifestations and pathophysiology of select disorders of the nervous system. a. Describe the risk factors, etiology, pathophysiology, and clinical manifestations of Parkinson’s disease, seizure disorder, multiple sclerosis, myasthenia gravis, and Guillain Barre. Parkinson’s disease (CNS disorder) Risk Factors: -After age 40 with mean onset of around age 60 -Males are more likely to develop Etiology: Unknown Pathophysiology Degenerative disorder of the basal ganglia resulting in the lack of the neurotransmitter dopamine. Begins with the degeneration of the dopamine-producing neurons in the basal ganglia and the corpus striatum. Dopamine is an inhibitory neurotransmitter and a deficiency 16 leads to an imbalance between dopamine and acetylcholine which is an excitatory neurotransmitter in the basal ganglia. The histologic features of the disease include depigmentation of the substantia nigra and Lewy bodies (damaged neurons). The basal ganglia are part of the diencephalon and works with the cerebellum to modify movements, specifically modify those movements transmitted via the extrapyramidal spinal tracts. These tracts are responsible for gross motor movements, facial expressions, posture, muscle tone, speech and swallowing. Usually presents after age 40 with the mean onset around age 60 Clinical Manifestations: Parkinsonism is a syndrome of abnormal movements that result from Parkinson’s or any disorder or drug that causes problems in the extrapyramidal tracts. Hypertonia, resting tremor, ridgity, bradykinesia or akinesia, dysphagia, abnormal posture-flexed forward, shuffling gait, mask-like face, weakness, drool, slurred speech and incontinence. Risk Factors: Seizure disorder Highest in childhood and old age (prognosis is good if patient adheres strictly to prescribed treatment Etiology: -cerebral lesions, cerebral trauma, idiopathic, genetic predisposition, perinatal injury, postnatal trauma, infection, brain tumor, vascular disease, congenital malformations, hypoglycemia, fatigue, lack of sleep, stress, fever, hyponatremia, constipation, use of stimulant drugs, ETOH withdrawal, withdrawal from depressant drugs, hyperventilation, and environmental stimuli (blinking lights, odors, loud noises) Pathophysiology The electrical balance at the neuronal level is altered, causing the membrane of the neuron to become easily activated. Increased permeability of the membranes help hypersensitive neurons fire abnormally. Abnormal firing may be activated by hyperthermia, hypoglycemia, hyponatremia, hypoxia or repeated sensory stimulation. When the intensity of a seizure discharge has progressed sufficiently, it spreads to adjacent brain areas. The midbrain, thalamus, and cerebral cortex are most likely to become epileptogenic (producing epileptic attacks) Excitement feeds back from the primary focus and to other parts pf the brain The discharges become less Clinical Manifestations: Auras: Pungent smell Nausea or indigestion Rising of sinking feeling in the stomach Dreamy feeling Unusual taste 17 Visual disturbance such as flashing lights Seizure activity Tonic stiffening followed by muscle contractions Tongue biting Incontinence Blank stare Purposeless motor activity Changes in LOC Loss of postural tone Jerking or twitching Multiple Sclerosis (CNS disorder) Risk Factors: -Caucasians -Females -Average age of onset is 20-40 Etiology: *Progressive CNS Disorder *Unknown, autoimmune disease Pathophysiology Results in the destruction of the CNS myelin. The PNS myelin is not affected in this disorder. More common in Caucasians and women. Average age onset is 20-40. It is an immune mediated process which begins with auto-reactive T and B cells which recognize the myelin sheath as an antigen. This triggers the immune and inflammatory response which leads to the destruction of the myelin sheath. The process only affects the gray and white matter of the CNS. This causes a progressive loss of function. When the axons demyelinate they transmit impulses much more slowly. Initially this process waxes and wanes. Eventually it is permanent. Clinical Manifestations: Paresthesia – numbness, tingling dysarthria (disorder of speech due to spasticity of the muscles used to speak) diplopia, blurred vision, bladder and bowel control issues, vertigo, ataxia, spasticity, quadriparesis, paraparesis 20 2. Generalized involve both cerebral hemispheres from the time of onset. Usually LOC and the whole body shows manifestation of the seizure. Clinical Manifestations: Absence: Blank stare and may or may not have automatism Clinical Implications: Clinical Manifestations: Tonic: (stiff) Muscle contraction with increased muscle tone. It is associated with the excitation of the thalamus and brain stem areas. Clinical Implications: Associated with excitation of the thalamus and brainstem Clinical Manifestations: Clonic: (jerking) Marked by quick repetitive jerks. It begins when the inhibitory neurons in the cortex, anterior hypothalamus and basal ganglia react to cortical stimulation Clinical Implications: Begins with inhibitory neurons in the cortex, anterior thalamus, and basal ganglia Clinical Manifestations: Tonic clonic: (Grand Mal) Experiences alternating stiffening and jerking movements. These individuals will be incontinent and disoriented or drowsy after the seizure. Clinical Implications: Loss of con. Incontinent, disoriented, or drowsy after seizure. Clinical Manifestations: 3. Status Epilepticus State of continuous seizures which last more than five minutes or seizures which rapidly occur before a patient reaches baseline, or one seizure that lasts >30 minutes. This is a medical emergency and can lead to permanent neurological injury. Clinical Implications: Medical emergency, Can lead to permanent neurological injury 21 4. Non-convulsive Status Epilepticus Clinical Manifestations: Usually presents without any signs of seizure activity. The patient will have an altered mental status that is not explained by any other cause. The only way to diagnose is by EEG. Clinical Implications: Can only be diagnosed with an EEG Central Nervous System Trauma 9. Analyze the etiology, clinical manifestations and pathophysiology of trauma of the central nervous system. c. Analyze the interdependence of normal cerebral hemodynamics and describe how they impact one another and affect ICP. Definition and normal values: Cerebral Blood Volume amount of blood in the intracranial vault at any given time. Usually 10% Effects of increased intracranial pressure: Increased ICP can result from an increase in intracranial content such as tumor growth, edema, excess CSF or hemorrhage. Necessitates an equal reduction in volume of other cranial contents. CSF most easily displaced, but if ICP remains high after CSF displacement then cerebral blood volume and flow will be altered. -Vasoconstriction and external compression of venous system in an attempt to decrease ICP Definition and normal values: Cerebral Blood Flow Cerebral blood flow (CBF) is normally regulated to meet the metabolic needs of the brain. It keeps the brain well oxygenated and is approximately 20% of the CO. this is 750-900ml of blood per minute. Cerebral blood flow is altered by the concentration of carbon dioxide and oxygen Effects of increased intracranial pressure: Ischemia. CBF decreases when CO2 decreases and it increases when the PaO2 is <50mmHg. CPP determines cerebral blood flow and is normal CPP (Cerebral Perfusion Pressure) is 60-100 mmHg. An alteration is either ICP or CPP will affect cerebral blood flow. 22 Cerebral Perfusion Pressure Definition and normal values: CPP is that pressure which is required to maintain perfusion of the brain. It is made up of ICP and the MAP. CPP determines cerebral blood flow and a normal CPP is 60-100 mmHg. Effects of increased intracranial pressure: An increased ICP will decrease the CPP and therefore impair cerebral perfusion. In the setting of elevated CPP, which can occur from HTN, there is an increase in hydrostatic pressure. The increased hydrostatic pressure causes fluid to move into the interstitium in the brain and causes ICP. This in turn, decreased CPP. Cerebral Oxygen Saturation Definition and normal values: Measured in the internal jugular vein (SJO2) at the jugular bulb and reflects the amount of oxygen still bound as blood leaves the cranial vault. Normal SjO2 is 55-70% Effects of increased intracranial pressure: The higher the intracranial pressure the less likely the CPP will be able to overcome it in order to bring needed oxygen to the brain. Definition and normal values: Intracranial Pressure ICP is the pressure in the intracranial vault. This pressure must be overcome in order for the brain to be perfused. A normal ICP is 5-15 mmHg or 60-180 mmHg H2O. Effects of increased intracranial pressure: Swelling causes an increased ICP which causes a decrease in CPP and brain ischemia occurs. This eventually causes cell death, the release of intracellular contents and contributes to the ICP. The ICP also blocks the flow of SCF in the cerebral ventricles and meninges, which causes the ventricles to swell and increases ICP, further decreasing CPP and causing more brain ischemia. ICP results from anything which increases the intracranial contents such as a tumor, edema, excess CSF, or hemorrhage. Cerebral compensation for ICP first starts with the dumping of the CSF. 25 d. Explain the pathophysiology of the primary and secondary brain injuries: Pathophysiology: Primary Injury Those injuries which directly injure the brain. They can cause neural damage, glial injury, shearing and rotation forces. Further divided into focal brain injuries and diffuse brain injuries. Pathophysiology: Secondary Injury Injury which occurs as a result of the mechanisms associated with the primary injury. Once the primary injury happens, inflammation sets in causing edema and tissue hypoxia. The swelling and hypoxia causes more damage. Other mechanisms of secondary brain injury include hypotension, hypoxia, anemia, hypo or hyperglycemia, hypercapnia, altered CBF, ischemia, inflammation, cerebral edema, decreased CPP and ICP and brain herniation. Tertiary brain injury develops after the acute event and usually days to months later. It results from complications such as pneumonia, fever, infection and immobility all which delay healing or contribute to more damage. e. Explain the differences between the four types (closed, open, focal, diffuse) of traumatic brain injuries. Definition: Closed Injury (blunt) Most common focal injury. Occurs when the head hits a hard, immobile surface or when a rapidly moving object strikes the head, like a baseball bat. The dura remains intact and the cranial contents do not come in contact with the environment. Will likely cause a concussion. Definition: Open injury (penetrating) Dura is damaged and the contents of the cranial vault are open to the environment. Basilar skull fracture is an example that usually involves the temporal bone. This allows CSF to leak from the ear canal and Battles sign (hematoma and swelling post auricular) Definition: Focal Injury Primary brain injury which is limited to one area of the brain. Definition: Diffuse Injury (diffuse axonal) Occurs from shaking force which strains the brain. This force causes a shearing, tearing and stretching of the nerve fibers and ultimately axonal damage. The person will end up with a concussion which may be mild, moderate or severe. 26 f. Describe the etiology, clinical manifestations and pathophysiology of focal and diffuse traumatic brain injuries. Coup Refers to the injury which lays directly under the area of impact. An injury to the frontal lobe usually results in only a coup injury Etiology: Occurs when the head strikes an immobile object, bounces off the object causing the brain to rebound to the opposite side of the original injury and strike the inside of the skull. Clinical Manifestations: Contusions and fractures. An injury to frontal lobe usually results in only a coup injury. Pathophysiology: Causes the brain to be injured at the site of impact and at the site opposite of the direct impact. This motion causes a shearing of the dural veins. Contrecoup Used to describe the occurrence of an injury on the opposite side of the impact. Usually characteristic of lateral and occipital direct impacts. Etiology: On the pole opposite the site of impact. Objects striking the back of the head or side of the head result in both coup and coutrecoup injuries because of the irregularity of the inner surface of frontal bones Clinical manifestations: This injury is characteristic of lateral and occipital direct impacts. Patho This causes the brain to be injured at the site opposite of the direct impact. Etiology: Contusions Found most commonly in frontal lobes, esp at the poles and along the inferior orbital surfaces; in temporal lobes, esp at anterior poles and along inferior surface, at the frontotemporal junction. Cause changes in attention, memory, executive attentional function (motivation, goal selection or formation, planning, self-monitoring, use of feedback), emotion, behavior Clinical Manifestations: May experience immediate LOC of more than 5 minutes, loss of reflexes, a transient loss of respirations, bradycardia and low BP. Vitals stabilize quickly. 27 Pathophysiology: Bruising of the brain tissue. Most common areas affected are the frontal and temporal lobes and frontotemporal junction. Results in brain edema, damaged neural tissues, increased ICP and necrosis of the contused area. 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 involves only events occurring several min prior to injury); symptoms >15 min - Grade III Any loss of consciousness (seconds-min); confusion and retrograde and anterograde amnesia remain present from impact and persist for several minutes Etiology: Headaches, anxiety, not feeling themselves, confusion and amnesia Clinical Manifestations: Initial confusional state last 1 to several minutes, possibly with amnesia for events preceding trauma (retrograde amnesia). Anterograde amnesia also may exist transiently. Head pain, complain of nervousness and “not being themselves” for up to a few days. There are 3 grades. Pathophysiology: The onset of confusion which may last one minute to several minutes. The individual will have a Glasgow coma score of 13-15 and may experience some amnesia. Classic Cerebral Concussion (Grade IV) *there are two forms: 1. Uncomplicated; without focal injury 2. Complicated; focal injury Ie: cerebral contusion that yields focal signs Etiology: Loss of reflexes, stop breathing, bradycardia, hypotension. Vital Signs quickly reverse. Head pain, nausea, fatigure and memory loss Clinical Manifestations: Transient cessation of respiration occur with brief periods of bradycardia, decrease in BP lasting <30 sec, VS stabilize within seconds to within normal limits. Confusional state lasts hours-days, head pain, nausea, fatigue. Attention/memory impaired for weeks to months, inability to concentrate and forgetfulness. 30 g. Differentiate between the etiology, clinical manifestations and pathophysiology of intracranial bleeds (epidural hematoma & hemorrhage, subdural hematoma, intracranial hematoma, subarachnoid hemorrhage) and describe the implications for clinical practice. Etiology: 1. Epidural Hematoma and hemorrhage Above the dura mater and between the skull is a potential space called the epidural space. Bleeds in this space are arterial in nature. Clinical Manifestations: Persistent, progressive, severe headache, vomiting, drowsiness, confusion, seizures and hemiparesis. An ipsilateral pupil dilation and contralateral hemiparesis reflects a temporal herniation. Pathophysiology: Collection of blood in that potential space between the skull and the dura mater. Bleeds are usually arterial in nature and therefore the bleeding is quicker. Can result in brain herniation and occurs in all age groups. 2. Subdural Hematoma MVA’s most common cause; 50% assoc with skull fx. - Acute (Rapidly develop within 48 hrs, usually located at top of skull (cerebral convexities) Etiology: Acute secondary to tearing of the veins and develop within hours - Chronic Etiology: Chronic bleeds typically occur after a fall or from chronic etoh abuse Found in older adults and those who abuse alcohol, some degree of brain atrophy with subsequent increase in the extradural space; develop in weeks to months Clinical Manifestations: Headaches, drowsiness, restlessness, slow cognition and confusion. May become worse as ICP increases. Will progress to a LOC, respiratory changes and pupil dilation Pathophysiology: Collection of blood between the dura mater and arachnoid mater. It is usually venous in nature and can be actute or chronic. Subacute bleeds develop within 48 hours to 2 weeks. Chronic bleeds are most common in the elderly and takes weeks to months to manifest symptoms. 31 3. Intracerebral Hematoma Etiology: Decreasing level of consciousness; coma or confusional state from other injuries, can make the cause of increasing unresponsiveness difficult to detect. Contralateral hemiplegia may occur. ICP rises. Usually assoc with MVA’s and falls from some distance Clinical Manifestations: Decreased LOC, confusion, coma, contralateral hemiplegia and brain herniation Pathophysiology: Intracranial bleed occurs directly into the cerebrum. Most commonly occurs in the frontal and temporal lobes. Because the hematoma is an expanding mass, it will compress the brain tissue and cause an increase in ICP 4. Subarachnoid Hemorrhage Etiology: HTN, cerebral aneurysms and head inuries Clinical Manifestations: Headache, changes in LOC, positive Kernig’s and Brudzinski’s signs and motor deficits. Cerebral vasospasms are a complication of SAH and can lead to delayed cerebral ischemia. Pathophysiology: Characterized by a bleed which occurs in the subarachnoid space. The space between the pia mater and the arachnoid mater. The bleeds causes an inflammatory reaction of the meninges. a. Discuss the etiology, pathophysiology and long term consequences of post concussive syndrome and chronic traumatic encephalopathy. Post Concussive Syndrome (PCS) occurs after mild traumatic brain injuries. It involves a constellation of symptoms which includes headaches, dizziness, neuropsychiatric symptoms and patient experience difficulties with learning, memory and attention. It most commonly occurs after mild TBIs but can occur with moderate or severe TBIs as well. One does not have to lose consciousness to develop this complication. PCS occurs in about 80% of persons with mild and moderate TBI. Women are at a higher risk for developing this syndrome. Also, the older one is the greater the risk for developing PCS. The pathophysiology is not well defined or understood. Patients with PCS will display global brain atrophy on imaging. Persons will also show signs of organic brain injury on imaging 1 year post TBI. Patients may experience PCS for 3-12 months after the initial TBI. In some instances, it will persist beyond 12 months. 32 Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disorder which results from repeated trauma to the brain. The pathologic hallmark of this disease is the deposition of tau (p- tau) protein throughout the brain. These individuals may initially present with chronic symptoms which include mood, cognitive, behavioral and motor disturbances. This diagnosis cannot be made definitively until after death and requires an autopsy. It is believed that the gene Apolipoprotein Eε4 (APOE ε4) increases the risk for developing CTE. Other risk factors include a prior concussion and previous history of headaches. Mortality from CTE and Alzheimer’s in retired National Football League players when compared to the general population is 3 times higher. College football players and soccer players are also at risk secondary to the sport. Professional boxers have been recognized to have chronic neurologic impairment as well. Pathologically these individuals have cerebral atrophy and extensive tau-immunoreactive degenerative changes which include neurofibrillary tangles, neutrophil threads and astrocytic tangles. There are four stages of CTE. Basically, the higher the stage the more widespread the tau protein accumulation is and the more severe the disease: • Stage I- p-tau neurofibrillary tangles are isolate to the sulcal depths of the cerebral cortex. • Stage II- is characterized by perivascular p-tau neurofibrillary tangles. • Stage III-p-tau deposition has spread to the frontal and temporal lobes. • Stage IV-is the most severe form of CTE and the p-tau protein is deposited widespread and involves the diencephalon, brain stem and cerebellum. Acute Intracranial Disorders 10. Analyze the etiology, clinical manifestations and pathophysiology of acute intracranial disorders. a. Differentiate between the risk factors, etiology, clinical manifestations and pathophysiology of thrombotic and hemorrhagic stroke. Thrombotic Stroke Risk factors: 1. Transient Ischemic Stroke Atherosclerosis & Inflammation A-Fib, left ventricular aneurysm or thrombus, left atrial thrombus, recent MI, rheumatic valvular disease, mechanical prosthetic valve, nonbacterial thrombotic endocarditis, bacterial endocarditis, patent foramen ovale, and embolic stroke Etiology: Clinical manifestations include persistent, progressive, severe headache, vomiting, drowsiness, confusion, seizures, and hemiparesis. An ipsilateral pupil dilation and contralateral hemiparesis reflects a temporal herniation 35 Area of Infarct: Vertebral Arteries Medulla and spinal cord tracts, anterior spinal artery, and penetrating branches (medial medullary syndrome) Clinical Manifestations: Motor- contralateral hemiparesis (face spared) and/or impaired contralateral proprioception; flaccid weakness or paralysis of the tongue and/or dysarthria Area of Infarct: Basilar Artery Serves the pons, medulla, lower midbrain, corticospinal and corticobulbar tracts and the ocular cranial nerve Clinical Manifestations: Quadriplegia, loss of voluntary facial, mouth and tongue movements, “locked-in syndrome” Posterior cerebral Artery Area of Infarct: Supplies the occipital love Clinical Manifestations: contralateral visual changes c. Describe the etiology, clinical manifestations and pathophysiology of migraine, cluster and tension headaches. Etiology: Migraine hormonal factors, family history, altered sleep patterns, missed meals, overexertion, weather changes, stress, menses, bright lights, strong smells, alcohol or nitrates Clinical Manifestations: Unilateral head pain, pulsating, pain worsening with activity, moderate to severe with nausea or vomiting, photophobia and phonophobia Patho: Episodic neurologic disorder whose marker is headache lasting 4-72 hours. Migraine is more common in those 25-55 years old and can occur in young children. The incidence is about 18% and 44% in females. 36 Cluster Etiology: Triggers similar to migraines Clinical Manifestations: Extreme pain of short duration, tearing on affected side, ptosis of the ipsilateral eye and congestion. Pain in periorbital and retrobulbar or temporal pain lasting 30 minutes to 2 hours. Lacrimation, reddening of the eye, nasal stuffiness, eyelid ptosis and nausea. Pain often referred to as midface and teeth. Patho: Trigeminal autonomic cephalgia. Occur primarily in men between 20-50 yo. Also known as a “histamine cephalagia”, “Horton syndrome” or “erythromelalgia”. They are uncommon and occur in clusters for a period of days followed by a long period of spontaneous remission. Mechanism for pain is related to the release of vasoactive peptides, the formation of neurogenic inflammation and activation of the pain matrix. Autonomic dysfunction is characterized by sympathetic underactivity and parasympathetic activation. Tension Etiology: (TTH) Not vascular or migrainous headache. Age is second decade. Onset of pain is gradual. Episodic TTH: several hours-days Chronic TTH: 15 days per month for 3 months. (treated with amitriptyline, cognitive behavior therapy, relax training.) Clinical Manifestations: Mild to moderate bilateral headache with a sensation of tight band or pressure around the head. It is localized. Patho: Probable genetic predisposistion. A central mechanism probably involves hypersensitivity of pain fibers from the trigeminal nerve that leads to central sensitization. The peripheral sensitization of myofascial sensory afferents may contribute to muscular hypersensitivity of and the development of chronic Tension headaches. 37 d. Explain the modes of transmission, etiology, clinical manifestations and pathophysiology of bacterial and viral meningitis and the implications for practice. Meningitis Fungi, Parasites, Toxins, aseptic 1. Bacterial and 2. Viral Mode of Transmission: Meningococcal is transmitted via air droplets and the individuals must be isolated for 24 hours after antibiotic therapy is started. Etiology: Most common causes for bacterial are meningococcus or pneumococcus. Aseptic meningitis is present when no causative agent can be found or refers to a viral etiology. Can also be viral, fungal or caused by TB. inflammation of brain or spinal cord. Infection may be acute, subacute, or chronic. Bacterial: meningococcus, pneumococcus. Viral: limited to meninges. No bacteria in spinal fluid. Enteroviral viruses, HSV2, arboviruses. Fungal: Chronic. Happens in impaired immune systems. Tubercular : common and serious CNS TB esp in AIDS. Clinical Manifestations: Photophobia, Kernig’s sign, Brudzinski’s sign, nuchal rigidity, focal neuro deficits, seizures Bacterial: -throbbing HA, Photophobia, nuchal rigidity, positive Kerning & Budzinski signs Viral: Mild compared to bacterial. -mild throbbing HA, photophobia, neck pain, stiffness, fever, malaise Fungal: Tubercular: headache, low grade fever, N&V, irritability, difficulty sleeping, fatigue. Confusion, stiff neck, behavior change, seizures. Patho: Infection of the meninges, specifically the pia mater Clinical Implications: Those that come into contact with meningococcal meningitis must be given prophylactic medications to prevent infection. Viral: treatment is supportive, resolves in 7-10 days