Caring for Clients With Neurologic and Spinal Cord Disorders 1 Dr Ibraheem Bashayreh, RN, PhD 4/1/2011 MEDICAL SURGICAL NURSING EPILEPSY A chronic neurologic disorder manifesting by repeated epileptic seizures (attacks or fits) which result from paroxysmal uncontrolled discharges of neurons within the central nervous system (grey matter disease). The clinical manifestations range from a major motor convulsion to a brief period of lack of awareness. The stereotyped and uncontrollable nature of the attacks is characteristic of epilepsy. 4/1/2011 DEFINITION 2 PATHOGENESIS The 19th century neurologist Hughlings Jackson suggested “a sudden excessive disorderly discharge of cerebral neurons“ as the causation of epileptic seizures. Recent studies in animal models of focal epilepsy suggest a central role for the excitatory neurotransmiter glutamate (increased in epi) and inhibitory gamma amino butyric acid (GABA) (decreased) 4/1/2011 3 EPIDEMIOLOGY AND COURSE Epilepsy usually presents in childhood or adolescence but may occur for the first time at any age. 4/1/2011 4 EPILEPSY is a symptom of numerous disorders, but in the majority of sufferers the cause remains unclear despite careful history taking,examination and investigation! 4/1/2011 5 EPILEPSY & SEIZURES Epilepsy is a neurological disorder characterized by recurring seizures 4/1/2011 also known as a “seizure disorder” A seizure is a brief, temporary disturbance in the electrical activity of the brain A seizure is a symptom of epilepsy 6 THE BRAIN IS THE SOURCE OF EPILEPSY • A seizure occurs when too many nerve cells in the brain “fire” too 7 quickly causing an “electrical storm” 4/1/2011 • All brain functions -including feeling, seeing, thinking, and moving muscles -depend on electrical signals passed between nerve cells in the brain EPILEPSY - CLASSIFICATION modern classification of the epilepsies is based upon the nature of the seizures rather than the presence or absence of an underlying cause. Seizures which begin focally from a single location within one hemisphere are thus distinguished from those of a generalised nature which probably commence in a deeper structures (brainstem? thalami) and project to both hemispheres simultaneously. 4/1/2011 The 8 EPILEPSY - CLASSIFICATION Focal seizures – account for 80% of adult epilepsies - Simple partial seizures - Complex partial seizures - Partial seizures secondarilly generalised Generalised seizures Unclassified seizures 4/1/2011 9 CLASSIFYING EPILEPSY AND SEIZURES Classifying epilepsy involves more than just seizure type 4/1/2011 Seizure types: Partial Simple Complex Consciousness is maintained Consciousness is lost or impaired Generalized Absence Convulsive Altered awareness Characterized by muscle contractions with or without loss 10 of consciousness GROUPS AT INCREASED RISK FOR EPILEPSY 4/1/2011 About 1% of the general population develops epilepsy The risk is higher in people with certain medical conditions: Mental retardation Cerebral palsy Alzheimer’s disease Stroke Autism 11 WHAT CAUSES EPILEPSY? about 70% of people with epilepsy, the cause is not known In the remaining 30%, the most common causes are: 4/1/2011 In Head trauma Infection of brain tissue Brain tumor and stroke Heredity Lead poisoning Prenatal disturbance brain development 12 SYMPTOMS THAT MAY INDICATE A SEIZURE DISORDER of blackout or confused memory Occasional “fainting spells” Episodes of blank staring in children Sudden falls for no apparent reason Episodes of blinking or chewing at inappropriate times A convulsion, with or without fever Clusters of swift jerking movements in babies 4/1/2011 Periods 13 SEIZURE TRIGGERS medication (#1 reason) Stress/anxiety Hormonal changes Dehydration Lack of sleep/extreme fatigue Photosensitivity Drug/alcohol use; drug interactions 4/1/2011 Missed 14 HOW IS EPILEPSY DIAGNOSED? 4/1/2011 Clinical Assessment Patient history Tests (blood, EEG, CT, MRI or PET scans) Neurologic exam ID of seizure type Clinical evaluation to look for causes 15 EPILEPSY DIFFERENTIAL DIAGNOSIS 4/1/2011 The following should be considered in the diff. dg. of epilepsy: Syncope attacks Cardiac arrythmias Migraine Hypoglycemia – seizures or intermittent behavioral disturbances may occur. Narcolepsy – inappropriate sudden sleep episodes Panic attacks PSEUDOSEIZURES – psychosomatic and personality disorders 16 EPILEPSY – INVESTIGATION concern of the clinician is that epilepsy may be symptomatic of a treatable cerebral lesion. Routine investigation: Haematology, biochemistry (electrolytes, urea and calcium), chest X-ray, electroencephalogram (EEG). Neuroimaging (CT/MRI) should be performed in all persons aged 25 or more presenting with first seizure and in those pts. with focal epilepsy irrespective of age. Specialised neurophysiological investigations: Sleep deprived EEG, video-EEG monitoring. 4/1/2011 The 17 TYPES OF TREATMENT 4/1/2011 Medication Surgery Nonpharmacologic treatment Ketogenic diet: a high-fat, adequate-protein, low-carbohydrate diet primarily used to treat difficult-to-control (refractory) epilepsy in children Vagus nerve stimulation Lifestyle modifications 18 EPILEPSY - TREATMENT 4/1/2011 The majority of pts respond to drug therapy (anticonvulsants). In intractable cases surgery may be necessary. The treatment target is seizure-freedom and improvement in quality of life! Basic rules for drug treatment: Drug treatment should be simple, preferably using one anticonvulsant (monotherapy). “Start low, increase slow“. Polytherapy is to be avoided especially as drug interactions occur between major anticonvulsants. The commonest drugs used in clinical practice are: Carbamazepine, Sodium valproate, Phenytoin (first line drugs) Lamotrigine, Topiramate, Levetiracetam, Pregabaline (new antiepileptic drugs AEDs) 19 EPILEPSY – TREATMENT (CONT.) pt is seizure-free for three years, withdrawal of pharmacotherapy should be considered. Withdrawal should be carried out only if pt is satisfied that a further attack would not ruin employment etc. (e.g. driving licence). It should be performed very carefully and slowly! 20% of pts will suffer a further sz within 2 yrs. 4/1/2011 If 20 EPILEPSY – SURGICAL TREATMENT of the pts with intractable epilepsy will benefit from surgery. Epilepsy surgery procedures: Curative (removal of epileptic focus) and palliative (seizure-related risk decrease and improvement of the QOL) Curative (resective) procedures: Anteromesial temporal resection, selective amygdalohippocampectomy, extensive lesionectomy, cortical resection, hemispherectomy. Palliative procedures: Corpus callosotomy and Vagal nerve stimulation (VNS). 4/1/2011 A proportion 21 STATUS EPILEPTICUS condition when consciousness does not return between seizures for more than 30 min. This state may be life-threatening with the development of pyrexia, deepening coma and circullatory collapse. Death occurs in 510%. Status epilepticus may occur with frontal lobe lesions (incl. strokes), following head injury, on reducing drug therapy, with alcohol withdrawal, drug intoxication, metabolic disturbances or pregnancy. Treatment: AEDs intravenously ASAP, event. general anesthesia with propofol or thipentone should be commenced immediately. 4/1/2011 A 22 POTENTIALLY DANGEROUS RESPONSES TO SEIZURE 4/1/2011 DO NOT Put anything in the person’s mouth Try to hold down or restrain the person Attempt to give oral anti-seizure medication Keep the person on their back face up throughout convulsion 23 23 MULTIPLE SCLEROSIS is an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are damaged, leading to demyelination and scarring as well as a broad spectrum of signs and symptom High risk groups Caucasian females Ages: 20–40 Family history Cold, wet, northern U.S. MULTIPLE SCLEROSIS Pathophysiology Autoimmune response with viral trigger Demyelination Spinal cord Brain Nerves of the CNS Myelin replaced with plaque Impulse transmission interrupted/ halted MULTIPLE SCLEROSIS (MS) Manifestations Exacerbations: Symptoms usually appear in episodic acute periods of worsening and remissions: is characterized by unpredictable relapses followed by periods of months to years of relative quiet (remission) with no new signs of disease activity. Progression longer exacerbations Triggers for exacerbations Heat Sun Infections Stress MULTISYSTEM EFFECTS OF MULTIPLE SCLEROSIS. MULTIPLE SCLEROSIS Long-Term Consequences Urinary tract infections Pressure ulcers/joint contractures Falls Pneumonia Depression MULTIPLE SCLEROSIS - MEDICATIONS Medications Immunomodulators Monoclonal antibody :are monospecific antibodies that are the same because they are made by identical immune cells that are all clones of a unique parent cell. Steroids Antispasmotics Urinary agents Pharmacotherapy for fatigue MULTIPLE SCLEROSIS – INTERDISCIPLINARY CARE Other Therapies Physical therapy Surgical intervention Neurectomy: is the surgical removal of a nerve or a section of a nerve Rhizotomy: is a neurosurgical procedure that selectively severs problematic nerve roots in the spinal cord, most often to relieve the symptoms of neuromuscular conditions. Plasmapheresis: is a blood purification procedure used to treat several autoimmune diseases Nutritional support MULTIPLE SCLEROSIS – CLIENT TEACHING Client/Family Teaching Triggers for exacerbations/stressors Medications/side effects Coping with deficits Counseling/support groups MULTIPLE SCLEROSIS – NURSING CARE Assessment Motor assessment Sensory changes Muscle strength; chewing/swallowing Tingling; vision changes Mood changes Urinary elimination patterns Past medical/family history MULTIPLE SCLEROSIS – NURSING CARE Assessment Respiratory effort ADLs Appearance MULTIPLE SCLEROSIS – NURSING CARE Nursing Diagnoses Fatigue Self-Care Deficit Ineffective Coping Impaired Mobility Risk for Injury MULTIPLE SCLEROSIS – NURSING CARE Evaluation ADL Coping Knowledge level Medications Diet Complications PARKINSON’S DISEASE Most common neurologic disorder in the U.S. 1.5 million affected Most common over age 40 Caucasian men vs. women PARKINSON’S DISEASE Pathophysiology Deficiency of dopamine Atrophy of cerebral cortex neurons Decreased dopamine receptors Loss of inhibition of acetylcholine Constant excitement of motor neurons PARKINSON’S DISEASE Manifestations of Parkinson’s Cardinal signs Tremor Rigidity Bradykinesia Tremor Rigidity of neck, shoulders, and trunk Bradykinesia: is characterized by slowness of movement Drooling : saliva flows outside the mouth PARKINSON’S DISEASE - MEDICATIONS Medications Dopaminergics Dopamine agonists Anticholinergics MAOIs PARKINSON’S DISEASE – INTERDISCIPLINARY CARE Other Therapies Surgery Pallidotomy: is a procedure where a tiny electrical probe is placed in the globus pallidus (one of the basal ganglia of the brain), which is then heated to to 80 degrees celsius for 60 s, to destroy a small area of brain cells Stereotactic thalamotomy: is an invasive procedure, primarily effective for tremors such as those associated with Parkinson's Disease (PD), where a selected portion of the thalamus is surgically destroyed (ablated). Deep brain electrical stimulation Complementary therapy Yoga Massage Acupuncture PARKINSON’S DISEASE – CLIENT TEACHING Client/Family Teaching Assistive devices Communication techniques Decreasing aspiration risk Safety Diet Exercise PARKINSON’S DISEASE – NURSING CARE Assessment Cognition, mood Motor functioning Falls; stiffness; jerking movements “Pill-rolling”: A circular movement or tremor of the tips of the thumb and the index finger when brought together. Facial muscle effects Weight loss; chewing/swallowing PARKINSON’S DISEASE – NURSING CARE Diagnoses Impaired Physical Mobility Impaired Verbal Communication Imbalanced Nutrition: Less than Body Requirements PARKINSON’S DISEASE – NURSING CARE Evaluation Ability to: Ambulate Chew and swallow Communicate Complications Knowledge level related to disease process MYASTHENIA GRAVIS is an autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatigability. Women ages 20–30 Exacerbations and remissions Triggers for exacerbations MYASTHENIA GRAVIS Pathophysiology Auto-antibodies from thymus gland Block acetylcholine receptors Decrease number of receptors Blockage of nerve impulses Face, lips, tongue, neck, and throat Can affect fine motor skills Can affect respiratory muscles MYASTHENIA GRAVIS Manifestations Ptosis (is a drooping of the upper or lower eyelid); diplopia (double vision) Slurred speech Difficulty chewing and swallowing Respiratory insufficiency Fatigue Altered facial expressions Difficulty writing MYASTHENIA GRAVIS Life-Threatening Complications Cholinergic crisis: is an over-stimulation at a neuromuscular junction due to an excess of acetylcholine (ACh), as of a result of the inactivity (perhaps even inhibition) of the AChE enzyme, which normally breaks down acetylcholine Severe muscle weakness, nausea, vomiting Salivation, sweating, bradycardia Myasthenia crisis: is a life-threatening condition, which is defined as weakness from acquired myasthenia gravis (MG) that is severe enough to necessitate intubation or to delay extubation following surgery . The respiratory failure is due to weakness of respiratory muscles. Muscle weakness Inability to swallow; respiratory distress MYASTHENIA GRAVIS - MEDICATIONS Medications Anticholinesterase medications Steroids Cytotoxic agents MYASTHENIA GRAVIS – INTERDISCIPLINARY CARE Short-Term Treatments Thymectomy Removal of the thymus Decreased auto-antibody production Plasmapheresis Removes auto-antibodies MYASTHENIA GRAVIS – CLIENT TEACHING Client/Family Teaching Medication regimen Strict time schedule Side effects CPR: airway management Symptoms of myasthenia and cholinergic crisis MYASTHENIA GRAVIS – NURSING CARE Assessment Muscle weakness Respiratory effort Ability to swallow Speech Vision SPINAL CORD INJURY – NURSING CARE Assessment Respiratory Rate, depth, effort Breath sounds Sensory level Elimination History of the trauma SPINAL CORD INJURY – NURSING CARE Diagnoses Ineffective Breathing Pattern Impaired Physical Mobility Impaired Urinary Elimination/Constipation Situational Low Self-Esteem SPINAL CORD INJURIES Affect adolescent and adult males Motor vehicle crashes Falls Violent acts Shootings Sports injuries SPINAL CORD INJURIES Pathophysiology Bruising or compression of cord via injury Bleeding into gray matter Inflammatory response Edema Hypoxia Ischemia No regeneration SPINAL CORD INJURIES Classifications Level of injury Cervical—tetraplegia: also known as quadriplegia, is paralysis caused by illness or injury to a human that results in the partial or total loss of use of all their limbs. Thoracic—paraplegia: is an impairment in motor or sensory function of the lower extremities Sacral Amount of cord damage Complete Incomplete SPINAL CORD INJURY Complications Decubitus (pressure) ulcers Pain, hypotonia, autonomic dysreflexia Spinal shock, orthostatic hypotension, bradycardia, deep vein thrombosis Limited chest expansion, pneumonia autonomic dysreflexia: is a potentially life threatening condition which can be considered a medical emergency requiring immediate attention. AD occurs most often in spinal cord-injured individuals with spinal lesions above the (T6) spinal cord level. Acute AD is a reaction of the autonomic (involuntary) nervous system to overstimulation. It is characterised by severe paroxysmal hypertension (episodic high blood pressure) associated with throbbing headaches, profuse sweating, nasal stuffiness, flushing of the skin above the level of the lesion, bradycardia, apprehension and anxiety, which is sometimes accompanied by cognitive impairment SPINAL CORD INJURY Complications Stress ulcers, paralytic ileus, stool impaction, stool incontinence Urinary retention, urinary incontinence, neurogenic bladder, urinary tract infections, impotence, decreased vaginal lubrication Joint contractures, muscle spasms, muscle atrophy, pathologic fractures, hypercalcemia SPINAL CORD INJURY Special complications Spinal shock: 30–60 minutes post injury Loss of reflex activity below injury Bradycardia and hypotension Loss of sweating and temp control Bowel and bladder dysfunction Flaccid paralysis SPINAL CORD INJURY Special Complications Autonomic dysreflexia Exaggerated sympathetic response SCIs T6 or above Involves triggers/stimuli Medical emergency CERVICAL SPINAL CORD INJURIES C1, C2, C3 no movement or sensation below the neck Ventilator-dependent C4 movement and sensation of head and neck; some partial function of the diaphragm CERVICAL SPINAL CORD INJURIES C5 controls head, neck, and shoulders; flexes elbows C6 uses shoulder, extends wrist. C7–C8 extends elbow, flexes wrist, some use of fingers THORACIC AND SACRAL SPINAL CORD INJURIES T1–T5 has full hand and finger control, full use of thoracic muscles T6–T10 controls abdominal muscles, has good balance THORACIC AND SACRAL SPINAL CORD INJURIES T11–L5 flexes and abducts the hips; flexes and extends the knees S1–S5 full control of legs; progressive bowel, bladder, and sexual function SPINAL CORD INJURY – INTERDISCIPLINARY CARE Emergent Care Airway, breathing circulation Pain; sensation Immobilization: neck, spine Oxygenation needs Intravenous fluids SPINAL CORD INJURY – INTERDISCIPLINARY CARE Diagnostic testing Cervical spine x-rays CT scan MRI SPINAL CORD INJURY – INTERDISCIPLINARY CARE Pharmacotherapy Corticosteroids Histamine blockers Anticoagulants Stool softeners SPINAL CORD INJURY – INTERDISCIPLINARY CARE Stabilization/immobilization Braces Body casts Cervical tongs/traction Halo vest SPINAL CORD INJURY – INTERDISCIPLINARY CARE Surgical interventions Spinal fusion Decompression laminectomy Insertion of rods HERNIATED DISK – INTERDISCIPLINARY CARE Treatment Medications for pain, muscle spasm; oral or injected corticosteroids Conservative treatment (body mechanics, exercises, firm mattress, warm moist compresses) Surgery: diskectomy, laminectomy, spinal fusion, microdiskectomy SPINAL CORD INJURY – NURSING CARE Assessment Respiratory Rate, depth, effort Breath sounds Sensory level Elimination History of the trauma SPINAL CORD INJURY – NURSING CARE Diagnoses Ineffective Breathing Pattern Impaired Physical Mobility Impaired Urinary Elimination/Constipation Situational Low Self-Esteem SPINAL CORD INJURY – NURSING CARE Evaluation Gas exchange/respiratory functioning Ability to manage ADL Bowel and bladder function Skin integrity Absence of system based complications TRIGEMINAL NEURALGIA Two sensory branches of the trigeminal nerve Pain along branches No known cause Dental procedure/surgery Facial trauma Infection Tumor TRIGEMINAL NEURALGIA Manifestations of Trigeminal Neuralgia Severe one-sided facial pain Stabbing/burning: forehead, nose, lips, cheek Exacerbations and remissions Simple actions can trigger symptoms TRIGEMINAL NEURALGIA MEDICATIONS Medications Anticonvulsant carbamazepine Phenytoin Baclofen