Patient with Neurologic Problems

1. Patient with Neurologic Problems By Linda Self

2. Rapid Neurologic Assessment • Glasgow Coma Scale • Response to painful stimuli—sternal rub, trapezius squeeze • Level of consciousness—even a subtle change is the first indicator of a declineinneurologic status • Decortication—abnormal posturing seen in the client with lesions that interrupt the corticospinal pathways. The patient’s arms, wrists, and fingers are flexed with internal rotation and plantar flexion of the legs.

3. Rapid Neurologic Assessment cont. • Decerebration-abnormal posturing and rigidity characterized by extension of the arms and legs,pronation of the arms, plantar flexion and opisthotonos (kind of spasm with head and feet bent backward and body bowed forward). Indicates dysfunction of the brainstem.

4. Rapid Neurologic Assessment cont. • Pupillary assessment, mental exam • Cranial nerve exam • Olfactory • Optic • Oculomotor • Trochlear • Trigeminal • Abducens • Facial • Acoustic • Glossopharyngeal • Vagus • Spinal accessory • hypoglossal

5. Brain Disorders—Migraines Caused by a phenomenon called “cortical spreading depression” whereby neurological activity is depressed over a specific area of the cortex—formerly felt to be related to dilation of cerebral blood vessels Results in release of inflammatory mediators leading to irritation of the nerve roots, especially the trigeminal nerve Serotonin release involved in the causation • Diagnosis is based on H&P, neurologic exam and imaging.

6. Migraines • Triggers • Tyramine-containing food and beverages such as beer, wine, aged cheeses, chocolate, yeast, MSG, nitrates, artificial sweeteners, smoked fish • Medications:estrogens, nitroglycerine, nifedipine, cimetidine • Other: fatigue, hormonal fluctuations, missed meals, sleeping problems, varying altitudes

7. Commonly Used Drugs for Migraines • NSAIDs • Beta blockers such as inderal • Calcium channel blockers-verapamil • Abortive drugs such as ASA, acetaminophen • Ergotamine preparations • Triptans • Opioids • Investigational—droperidol (Inapsine)

8. Seizures • Abnormal, sudden, excessive, uncontrolled electrical discharge of neurons within the brain. May cause change in LOC, motor or sensory ability, and/or behavior. • Epilepsy—chronic disorder characterized by recurrent, unprovoked seizure activity

9. Types of Seizures • Generalized • Absence—petit mal • Tonic-clonic—grand mal. Muscle stiffening followed by jerking • Myoclonic—contractions of body muscles • Atonic—go “limp”, drop attacks • Partial—simple partial, complex partial • others

10. Antiepileptic Drugs • Tegretol—partial or generalized seizures • Klonopin—absence, myoclonic and akinetic seizures • Valium—status epilepticus • Depakote—all types • Zarontin-absence seizures • Neurontin—partial seizures • Dilantin-all types • Topamax—for intractable partial seizures • Keppra—adjunct in partial seizures

11. Common side effects of anti-epileptics (AEDs) • Teratogenic potential • Medication interactions • Blood dyscrasias • Altered liver function • Effects on renal function • Wt. gain or loss • Sometimes sedation

12. Surgical options • Identify seizure area by EEG, insert electrodes, surgically excise • corpuscallostomy

13. Characteristics of Seizures Important to observe and document: • How often? • Description • Progression • Duration • Last time occurred • Preceded by aura? • What does patient do post-seizure? • Time elapsed before returns to baseline

14. Seizure Precautions • Stay with patient • O2 • Airway • Suction • IV access • Siderails up, padded • Bed in lowest position • Turn patient to side • Loosen restrictive clothing • Do not force anything into the mouth • Following seizure—do neuro checks

15. Status Epilepticus • Characterized by prolonged seizures lasting more than 5 minutes or repeated seizures over the course of 30 minutes • Is a medical emergency. Brain damage and death can ensue. • Untreated can cause hypoxia, hypotension, hypoglycemia, dysrhythmias and lactic acidosis. Rhabdomyolysis can occur with effects on the kidneys.

16. Treatment of Status Epilepticus • Lorazepam is the drug of choice due to rapid onset of action and long duration of action • Valium • Phenobarbital • Dilantin • Supportive/safety care

17. Meningitis • Inflammation of the meninges or brain covering • Entry is via the bloodstream at the blood-brain barrier. May be direct route or via skull fracture. Exudate will develop. • Viral is most common • Fungal-Cryptococcal. Can be caused by sinusitis • Bacterial-mortality rate+25%. Most commonly caused by Neisseria meningitidis and Streptococcus pneumoniae.

18. Meningitis—S/S • LOC • Disorientation • Photophobia • Nystagmus • hemiparesis • CN dysfunction • Personality changes • N/V • Fever and chills • Red macular rash • Nuchal rigidity, positive Kernig’s (hamstring pain w/extension) and Brudzinski’s (flexion of the hips when the neck is flexed)

19. Review of CSF findings • Pressure <20cm of H2O • Clear, colorless. Cloudy indicates infection. Pink to orange==RBCs • Cells 0-5 lymphocytes normal. • Glucose—50-75mg/dL normal, less than 50 indicates infection • Proteins 15-45 normal, 45-100 paraventricular tumor, 50-200 viral, more than 500=bacterial infection

20. Meningitis cont. • CSF findings: • Bacterial—cloudy, increased WBCs, increased protein, decreased glucose, elevated CSF pressure >180mm h20 • Viral—clear, increased WBCs, slighly elevated protein, normal glucose, variable CSF pressure

21. Meningitis • May display s/s of increased ICP ( see following slide) • Left untreated, can result in brain herniation or damage

22. Meningitis • Treatment according to causative pathogen as found by LP (lumbar puncture) • Bedrest • IV fluids, analgesics for pain and fever • Anticonvulsants • Corticosteroids • Pathogen specific abx—meningococcus penicillin or cephalosporins, contacts rifampin or cipro; pneumococcal—PCN, cephalosporins and also vancomycin

23. ICP • Pressure-volume relationship between ICP, volume of CSF, blood, brain tissue and cerebral perfusion pressure (Monroe-Kellie Hypothesis) • Cranial compartment is incompressible and cranial contents should have a fixed volume • Equilibrium must be maintained. Increased volume will result in downward displacement of the brain

24. Key Features of Increased Intracranial Pressure • Lethargy to coma • Behavioral changes • Headache • N/V • Change in speech pattern • Aphasia • Pupillary changes--papilledema • Cranial nerve dysfunction • Seizures • Abnormal posturing • Cushing’s Triad—elevatedBP,decreased pulse anddecreased respirations

25. Treatment of increased ICP • Maintain airway • Hyperventilate patient to “blow off” CO2 (CO2 dilates blood vessels) • Raise HOB to allow for venous drainage • Decrease metabolic demands by paralyzing and sedating patient • Mannitol • corticosteroids • Pain management • Intracranial monitoring (in ventricle) • Craniotomies • Decompressive craniectomy

26. Brain Attacks (Strokes or CVAs) • Affects over 550, 000 Americans per year • Two major types—ischemic and hemorrhagic • Caused by disruption of the normal blood supply to the brain • May be preventable if causes discovered early

27. Risk Factors for Brain Attacks • Obesity • Heart disease • Diabetes mellitus • Hypercholesterolemia • Hypercoagulable states • Cocaine, illicit drug use • Atrial fibrillation

28. Differential Features of the Types of Stroke Thrombotic—onset is gradual • Usually related to ASHD and hypertension • Intact LOC • May have speech and visual changes • Slight HA • No seizures • Deficits may be permanent

29. Differential of strokes Embolic • Abrupt • Steady progression • Awake • May be associated with cardiac disease • Maximal deficits at onset • No seizures • Rapid improvements

30. Differentials of strokes Hemorrhagic • Sudden onset • Deepening stupor or coma • May have hypertension • Focal deficits • Seizures possible • Permanent deficits possible • May result from an aneurysm, rupture of an AV malformation or severe hypertension

31. Ishemic Stroke • Caused by a blockage of a blood vessel • Generally caused by atherosclerosis • Early warning signs include: transient loss of vision, transient ischemic attack (called silent strokes) • Risk factors: atrial fibrillation, ASHD, cocaine use/abuse, hx of “blood clots” • Treatment—”clot buster” TPA, streptokinase,others

32. Transient ischemic attack vs. reversible ischemic neurologic deficit • Ischemic strokes are often preceded by warning signs such as TIAs or RINDs • Both cause transient focal neurologic dysfunction from a brief interruption in cerebral blood flow • TIAs last minutes to <24h • RINDs last >24h but less than a week

33. Hemorrhagic strokes • If survive event, recovery from hemorrhagic stroke better than ischemic • Caused by vascular disruption e.g. aneurysms, AVM • Surgical decompression

34. Assessment of patient with brain attack • Neurologic exam • Motor exam—hemiplegia vs. hemiparesis • Sensory changes-neglect syndrome (most notable in right cerebral hemispheric injuries) • Amaurosis fugax—temporary loss of vision in one eye • Hemianopsia—blindness in one half of visual field • Cranial nerve function • Cardiovascular assessment—abrupt reduction of BP not advised

35. Assessment • Baseline CT, MRI even better (want to ensure that the stroke is not hemorrhagic) • ECG • Echocardiogram • Cardiac enzymes

36. Interventions Depending of type of brain attack: • Anticoagulants (assuming not a bleed) • Catheter directed thrombolytic therapy—may use if systemic tx not effective • Endarterectomy • Craniotomy • Systemic thrombolytic tx—must meet strict criteria. Must give within 3hours of onset of s/s • Wire coils in aneurysms—seals the area

37. Key considerations • Impaired physical mobility; self care deficit • Disturbed sensory perception • Unilateral neglect—in rt cerebral stroke. May have lack of proprioception and failure to recognize their impairment • Impaired verbal communication—expressive aphasia (Broca’s), receptive aphasia (Wernicke’s)

38. Parkinson’s disease • Genetic and environmental contributors • Associated with four cardinal s/s: tremor, rigidity, akinesia (slow movements), and postural instability • Degeneration of substantia nigra—decreased dopamine. Acetylcholine will predominate. Also with norepinephrine loss thus the postural hypotension.

39. Parkinson’s Key Features • Stooped posture • Slow and shuffling gait • Pill-rolling, mask-like facies, uncontrolled drooling, rare arm swinging with walking • Change in voice, dysarthria and echolalia • Labile and depressed, sleep disturbances • Oily skin, excessive perspiration, orthostatic hypotension

40. Parkinson’s Disease Stages • Initial-hand and arm trembling, weakness, unilateral involvement • Mild-masklike facies, shuffling, bilateral involvement • Moderate—increased gait disturbances • Severe—akinesia, rigidity • Complete dependence

41. Interventions • Eldepryl (MAO inhibitor which decreases the breakdown of dopamine) • Dopamine agonists—stimulate dopamine receptors but have side effects such as nausea, drowsiness, postural hypotension and hallucinations. Mirapex and Requip mimic the actions of dopamine.

42. Interventions cont. • Levodopa/carbidopa. Used as disease progresses. “Wearing off” phenomenon. • Amantadine—used to treat the “wearing off” s/s. • Stavelo—(carbidopa/levodopa/entacapone). Dopa-decarboxylase inhibitor/dopamine precursor/COMT inhibitor. Useful in end-stage disease.

43. Drug toxicity/tolerance in PD • Reduce medication dosage • Change of medications or in the frequency of administration • Drug holiday up to 10 days

44. Nursing considerations • Maintain mobility and flexibility by ROM • Encourage self-care as much as possible • Monitor sleep patterns to avoid injury • Nutrition-may need soft or thickened foods. • Constipation • Speech therapy may be needed • Psychosocial support—impaired memory cognition

45. Surgical Management in PD • Stereotactic pallidotomy • Deep brain stimulation when meds no longer work. Electrode is implanted and connected to a “pacemaker” in chest. • Fetal tissue transplantation using fetal substantia nigra (implanted in the caudate nucleus of the brain).

46. Alzheimer’s Disease • Chronic progressive degenerative disease usually seen in individuals older than 65 • Characterized by loss of memory, judgment, and visuospatial perception and by a change in personality • Progressively physically and cognitively impaired resulting ultimately in death

47. AD • Increased amount of beta amyloid • Neurofibrillary tangles throughout the neurons • Neuritic plaques • Granulovascular degeneration • Reduced levels of acetylcholine • ? Increased levels of glutamate

48. Key Features of AD • Early-forgets names, misplaces household items, mild memory loss, short attention span, subtle changes in personality, wanders, impaired judgment • Middle—cognition vitally impaired; disoriented to time, place and event; agitated; unable to care for self, incontinent • Severe-incapacitated; motor and verbal skills lost

49. Physical Assessment of AD • Observe for stage of progression • Observe for changes in cognition—attention, judgment, learning and memory, communication/language • Observe for changes in behavior • Changes in self-care skills • Psychosocial assessment • Dx of exclusion. Check CMP, CBC, B12, folate, TSH, RPR, drug toxicities and levels, alcohol screening • PET or MRI to r/o pathology

50. Mini-mental state examination—orientation, registration (repeat three words), naming, reading and following directions. • Good one is to have them draw a clock with an indicated time