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M6 13-005
Exam 15: Common Neurological Disorders
| Term | Definition |
|---|---|
| Headaches and their characteristics | Common neurological complaint with variable clinical significance. Results from a variety of causes. (Source must be determined with careful physical examination and appropriate neurological assessment). Exact mechanism of head pain unknown. |
| Headaches: Pain arises from | Scalp, its blood vessels and muscles. Dura mater and its venous sinuses. Blood vessels at the base of the brain. Cervical cranial nerves. |
| Headaches: Classified as | Vascular. Tenison. Traction-inflammatory. |
| Vascular Headache | Migraine. Cluster. Hypertensive. |
| Tension Headache | Psychological cause (tension or stress). Medical cause (cervical arthritis). |
| Traction-inflammatory Headache | Infection, intracranial or extracranial causes. Occlusive vascular structures. Temporal arteritis. |
| Clinical Manifestations of a migraine (Prodromal S&S) | 1) Visual field defects. 2) Experiencing unusual smells or sounds. 3) Disorientation. 4) Paresthesias. 5) Paralysis of a part of the body (rare). |
| Clinical Manifestations of a migraine (During Migraine) | 1) Nausea, vomiting. 2) Sensitivity to light. 3) Chills, diaphoresis. 4) Irritability, fatigue. 5) Edema. |
| Diagnostic Tests for Headache | (1) Neuro exam, CT, MRI, X-rays. (2) A lumbar puncture may be done in the absence of a brain tumor or increased ICP. (Rapid reduction of intracranial pressure by LP may cause herniation). In these cases a CT scan must be done first. |
| Neuropathic Pain (Other than headache) may evolve from lesions involving | 1) Peripheral cutaneous nerves. 2) Sensory nerve roots. 3) The thalamus. 4) Central pain tract. |
| Pain receptors are not adaptable and are specific for pain only | not adaptable and are specific for pain only |
| Pain continues | as long as stimuli is present. |
| Pain receptors can be activated by: | (a) Cellular damage. (b) Innate chemicals (such as histamine). (c) Heat/cold. (d) Ischemia. (e) Muscle spasms. (f) Pruritus. |
| Intractable pain | Pain that is unbearable and does not respond to treatment |
| Neurolpathic pain Dx tests | Electrical stimulation (used to define pain). Psychological testing. Myelogram -(used for back or neck pain). |
| Non-surgical pain control | Transcutaneous electrical nerve stimulation (TENS) or Spinal cord stimulation. Nerve block (used for intractable pain). Medications. Counseling. |
| Neurectomy | nerve excision. |
| Rhizotomy | cut of a spinal nerve root. |
| Cordotomy | cutting a nerve in the spinal cord. |
| Percutaneous cordotomy | destruction of a nerve bundle by means of an electric current. |
| Increased Intracranial Pressure: | a) potential complication in many neurological conditions. (b) Often occurs suddenly and progresses rapidly. (c) Can lead to death if untreated. |
| Causes of increased ICP | (a) Space occupying lesions (tumors). (b) Trauma/Hemorrhage. (c) CSF excess (due to tumor or inability to drain). (d) Cerebral Edema (due to tumor, trauma, hypoxia). (e) Encephalopathy |
| pressure increases within the cranial cavity compensation occurs by: | 1) Venous compression and displacement. a) As pressure increases blood flow is decreased. b) This results in inadequate tissue perfusion. 2) CSF displacement to the spinal cord. 3) Supratentorial shift (brain herniation). |
| Inadequate tissue perfusion results in: | 1) ↑ PaC02 and decreased pH and Pa02. These changes result in vasodilation, edema and impaired cellular function. 2) ↑ edema leads to even greater ICP, further decreased in blood flow and worsening tissue ischemia (results in vicious cycle). |
| Herniation of the brain can occur resulting in compression of: | 1) Vasomotor center. 2) Posterior cerebral artery. 3) Oculomotor nerve. 4) Corticospinal nerve pathway. 5) Fibers of the ascending reticular activating system.(controls wake and sleep states). |
| Clinical Manifestations of Increased ICP: Initial | Initially exhibit little or no change in clinical presentation, depending on etiology. |
| Clinical Manifestations of Increased ICP: Most important role for nurse | detection of change, in order to intervene while it is still reversible. (Frequent observation and assessment is critical!). |
| Deterioration of LOC (level of consciousness) early sign w/ ICP | 1) Reliable and sensitive. 2) Confusion, restlessness, lethargy, coma. |
| Pupillary dysfunction w/ ICP | Size changes occur on the ipsilateral (same) side of lesion. Progresses from constriction to dilation. Results from loss of parasympathetic input from the oculomotor nerve (CN III). Terminal stage is dilated, fixed pupils due to compression of CN III. |
| Visual Abnormalities w/ ICP | 1) Visual deficits can develop in early stages of IICP: decreased visual acuity, blurred vision and diplopia (early sign) quite common. 2) As ICP rises the ocular symptoms will usually become more pronounced. |
| Clinical Manifestations of Increased ICP: Headache | (a) Pain increases with coughing, straining, or stooping. (b) Often occurs early in the morning and may awaken patient. |
| Clinical Manifestations of Increased ICP: Alteration in Blood Pressure and Pulse | Early stages: BP and P remain relatively stable. Increased systolic blood pressure and later decreasing diastolic blood pressure, both resulting in widening pulse pressure. As ICP continues to rise, patient deteriorates and decompensation begins. |
| Cushing's syndrome | A widen pulse pressure, increased systolic BP, and bradycardia. |
| Clinical Manifestations of Increased ICP: Alteration in Respirations | Alterations in characteristics of respiratory pattern relate to level of brain dysfunction. Snore-like. Cheyne Stokes. Ataxic (irregular and unpredictable breathing pattern with random, shallow and deep breaths with occasional pauses). |
| Clinical Manifestations of Increased ICP: Alteration in Temperature (due to compression of thermoregulatory center). | Temperature usually associated with hypothalamic dysfunction. In the compensatory phase – Temperature probably WNL. In decompensatory phase - Temperatures at very high levels are frequently observed (increases brain metabolism and worsens condition). |
| Clinical Manifestations of Increased ICP: Loss of Brain Stem Reflexes | Late stages – pressure on brain stem causes loss or dysfunction of reflexes mediated by the brain stem. Babinski's reflex. Hyerreflexia. Rigidity. Seizures. Posturing (Decorticate or Decerebrate). |
| Decorticate. | a) Flexion of arms, wrists and fingers with adduction in upper extremities. b) Extension, internal rotation and plantar flexion in lower extremities. |
| Decerebrate: | a) All four extremities in rigid extension with hyperpronation of forearms and plantar extension of feet. |
| Clinical Manifestations of Increased ICP: Papilledema | Swelling of the optic disc. -Late finding with ICP. Does not occur until ICP has reached markedly elevated levels. -Not a universal observation usually noted by MD on exam. -In some patients this may be first sign. |
| Clinical Manifestations of Increased ICP: Other S&S | (a) Projectile vomiting. (b) Singultus (hiccups- caused by compression of the vagus nerve). |
| ICP Medical Treatment: Pharmacological | 1) Hyperosmotic agents (Mannitol). 2) Sedation (Versed or Tracrium). 3) Corticosteroids (Decadon) 4) Prevention of GI Ulcers (Antacids) 5) Anti-Convulsants (Dilantin, Cerebyx) |
| ICP Medical Treatment: Mechanical | Craniotomy. Craniectomy. Drainiage of Ventricles or subdural hematoma. |
| Craniotomy | Bone flap removed and replaced (for example, removal of a tumor). |
| Craniectomy | Bone flap removed and not replaced (often used in trauma to allow brain to swell out of hole). |
| ICP Medical Treatment: Endotracheal Intubation | Used in severely injured patients to maintain therapeutic PaO2 and PaCO2. Hypoxia produces cerebral vasoconstriction and is, therefore, avoided. Hypercarbia (elevated PaCO2) causes an increase in ICP. PaCO2 is maintained in the normal range |
| Motor Function Disturbance | Results from damage to the nervous system. Patients often have significant problems with mobility (An example is a patient with cerebral palsy). |
| Motor Function Disturbance: manifestations | (1) Alteration in: (a) Muscle strength. (b) Muscle tone - flaccid or hyperreflexic. (c) Reflex activity. (2) Manifestations differ according to neurological lesion .Ex: Flaccid vs. Hyperreflexic |
| Motor Function Disturbance: Diagnostic Test | Electromyogram |
| Electromyogram | Applying surface electrodes or inserting needle electrodes into a muscle to observe electrical activity. Detects various types of electrical activity and abnormal patterns seen in pathology. |
| Motor Function Disturbance: Medical Management (Spasticity) | Muscle relaxants (with side effects of drowsiness and vertigo). -Baclofen. -Dantrolene. -Valium. |
| Motor Function Disturbance: Medical Management (Dysphagia) | 1) Aspiration precautions. 2) Prefeeding and feeding exercises. 3) With Severe aspiration risk, video fluoroscopy with barium. |
| Motor Function Disturbance: Medical Management (Paralysis) | Protect the affected area. 1) Eyes. 2) Limbs. |
| Alteration in sensory and perceptual function. | Disruption in the sensory system pathway from the receptor to the sensory cortex by a lesion. Alters the transmission or perception of sensory information. Results in difficulty with daily functioning and decreased ability to protect self from injury. |
| Proprioception | ability to know the body position without looking directly at it. |
Created by:
jtzuetrong
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