Neurological Disorders PDF

# Neurological Disorders ## Introduction A wide variety of disorders involving breakdown or progressive dysfunction of nerve cells. Causes a slow and progressive loss of independence. ### Degenerative Diseases - Parkinson's - Multiple Sclerosis - Myasthenia Gravis ## Parkinson's - Chronic,...

# Neurological Disorders ## Introduction A wide variety of disorders involving breakdown or progressive dysfunction of nerve cells. Causes a slow and progressive loss of independence. ### Degenerative Diseases - Parkinson's - Multiple Sclerosis - Myasthenia Gravis ## Parkinson's - Chronic, progressive neurodegenerative disorder characterized by slowness in the initiation and execution of movement (bradykinesia), increased muscle tone (rigidity), tremor at rest, and gait changes. - There is a deficiency of dopamine in the basal ganglia, which is the mid-lower part of the brain that controls motor function. - Dopaminergic neurons in the substantia nigra are destroyed. - Cause is unknown. ### Manifestations #### Tremor - Tremor is often the first sign. - Most visible manifestations. - Parkinsonian tremor is more prominent at rest. - The hand tremor is described as "pill rolling" because the thumb and forefinger appear to move in a rotary fashion as if rolling a pill, coin, or other small object. - Appears intermittently; disappears during sleep. #### Rigidity - Rigidity is the increased resistance to passive motion. - Parkinsonian rigidity is typified by a jerky quality (cogwheel rigidity). - Results in muscle soreness. - Begins unilaterally but then progresses over time. #### Akinesia/Bradykinesia - Akinesia is the absence or loss of control of voluntary muscle movements. - In PD, bradykinesia (slowness of movement) is especially evident. - Masked face (deadpan expression). - Speech becomes slower. ### Other signs and Symptoms: - Impaired swallowing. - Decreased autonomic function. - Reduced blink. - Shuffling gait. - Stooped posture. ### Assessment - Observe for characteristics. - Perform orthostatic blood pressure and pulse readings. - Mental status exam. - Assess cranial nerves. ### Diagnostic Studies - Because no specific diagnostic test exists for PD, diagnosis is based on the patient's history and clinical features. - Clinical diagnosis requires the presence of TRAP (tremor, rigidity, akinesia, and postural instability) and asymmetric onset. - Confirmation of PD is a positive response to antiparkinsonian drugs (levodopa or DA agonist). - MRI and CT have a limited finding in diagnosis of PD because they do not show a specific pathologic finding. However, they can rule out a stroke or brain tumor. ### Treatment - Maintain quality of life and improve functional disability. - Avoid or minimize side effects. - Control symptoms. #### Medications Therapy - Aimed at correcting the imbalance of neurotransmitters. - Eldepryl - retards progression of disease - Dopamine agonists: stimulate dopamine receptors in the brain. - Symmetrel (selegiline) - Mirapex (pramipexole) - Parlodel (bromocriptine) - Artane - Anticholinergic receptors: - Cogentin - Levodopa - can have on/off periods where the medication will stop being therapeutic - Siminet - 1st line of choice - SSRIs to treat depression and anxiety. - Can progress to dementia-like s/s. ### Nursing Implementation - Because PD is a chronic degenerative disorder with no acute exacerbations, teaching and nursing care are directed toward maintaining good health, encouraging independence, and avoiding complications, such as contractures and falls. - Problems due to bradykinesia can be addressed by relatively simple measures. - A physical therapist can design a personal exercise program to strengthen and stretch specific muscles. - Safety!! - Incorporate environmental changes to prevent falls. ## Multiple Sclerosis - Multiple sclerosis (MS) is an autoimmune, degenerative disorder of the CNS characterized by: ### Inflammation - Reduces the thickness of myelin sheath and impulse conduction is slowed/blocked. ### Demyelination of Motor Neurons - Scattered demyelination - Possibly caused by viral infection that intiates autoimmune respons. - T-cells attack the fatty myelin sheath and the nerve fiber is broken ### Classifications - **Relapsing - remitting:** - Cycles of exacerbation and remission with a slow progression of disease over time. - **Primary - progressive:** - Linear progress of disease. - **Secondary - progressive:** - Phases of exacerbations and remissions followed by progression of disease.. - **Progressive relapsing:** - Progressing with exacerbations. ### Clinical Manifestations - Highly variable and unpredictable. - Sites of demyelination occur anywhere throughout the brain and spinal cord. - Wide range of signs and symptoms: - **Cranial nerve dysfunction:** - Diplopia. - Dysphagia. - Facial weakness. - **Motor dysfunction:** - Weakness. - Paralysis. - Spasticity. - Abnormal gait. - **Cerebral dysfunction:** - Dysarthria. - Tremor. - Incoordination. - Ataxia. - **Bowel/bladder dysfunction:** - Fecal and urinary urgency. - Constipation. - Incontinence. - **Cognitive:** - Decreased short term memory. - Mood alterations - usually have to be on antidepressants. - **Sexual Dysfunction:** - **Fatigue - overwhelming weakness** ### Diagnostic Studies - There is no definitive diagnostic test for MS, the history, manifestations, and results certain diagnostic tests are important. - An MRI of the brain and spinal cord may show white matter lesions. - Immunoglobulin G may be elevated. - Autoimmune biomarker. ### Drug Therapy - Goal of therapy is to decrease inflammation and destruction of myelin sheaths. - Treat acute attacks. - Decrease number of relapse. - Immune response control. - Prednisone. - Medrol. - ACTH (corticotropin). - Copaxone. - Symptom management: - Stool softeners. - Tremors: Inderal (propranolol). - Incontinence: Ditropan. ### Nursing Implementation - The patient with MS should be aware of triggers that may cause worsening of the disease. - These include infection (especially upper respiratory and urinary tract infections [UTIs]), trauma, immunization, childbirth, stress, and change in climate. - During an acute exacerbation, the patient may be immobile and confined to bed. The focus of nursing interventions at this phase is to prevent complications of immobility. - Focus patient teaching on general resistance to illness. This includes avoiding fatigue, extremes of heat and cold, and exposure to infection. ## Myasthenia Gravis (MG) - Myasthenia gravis (MG) is an autoimmune disease of the neuromuscular junction marked by fluctuating weakness of certain skeletal muscle groups. ### Etiology and Pathophysiology - MG is caused by autoimmune process in which antibodies attack ACh receptors. - This results in fewer ACh receptor (AChR) sites at the neuromuscular junction and results in weakness and fatigue. - Muscle contraction is contingent upon acetylcholine, in MG, the number of receptors are significantly reduced. ### Manifestations - Ocular muscles are the first to be affected. - Diplopia and ptosis(dragging of the eyelid). - Muscles of the face, chewing, speech, swallowing, and neck muscles are the next significant changes. - Generalized weakness is most prominent symptom. ### Diagnostic Studies - AChR antibody titer test: elevated. - EMG - detects transmission delay or failure in muscle fibers to send impulses. Thymus MRI- might be thymus gland involvement. - Tensilon test can indicate MG. - A patient with MG has rapid improvement in muscle strength after IV injection of Edrophonium. Edrophonium is an anticholinesterase agent. It blocks the enzyme acetylcholinesterase, the enzyme that breaks down ACh. ### Treatment - There is no cure but it is managed well with early treatment and drug therapy. - Anticholinesterase drugs: - Enhance transmission at the neuromuscular junction. - Pyridostigmine (Mestinon) - Corticosteriods: - Prednisone - Immunosuppressants: - Cyclosporine (Sandimmune) ### Nursing Implementation - Nursing care is aimed at maintaining adequate ventilation, continuing drug therapy, and watching for side effects of therapy. - Might present to the hospital with features of a cholinergic crisis include involuntary muscle contraction, sweating, excessive salivation, and constricted pupils. - As with other chronic illnesses, focus care on the neurologic deficits and their impact on daily living. - Teach the patient about a balanced diet that can easily be chewed and swallowed. ## Bell's Palsy - Bell's palsy is an acute, usually temporary, facial paresis (or palsy) resulting from damage or inflammation of the facial nerve (CN VII/7). - It usually affects only one side of the face, but both sides can be affected. ### Pathophysiology - Cause is unknown. - Believed to be a reactivation of herpes simplex virus isoform (HSV-1) and/or herpes zoster virus (HZV). - Risk factors: - Pregnancy. - Family history. - HTN. - DM. ### Clinical Manifestations - The key feature of Bell's palsy is the acute onset of unilateral lower motor facial weakness. - 50% to 60% have pain around and behind the ear and neck. - Other manifestations include drooping of the eyelid and corner of the mouth, drooling, facial twitching, dryness of the eye or mouth, facial numbness, altered taste. ### Treatment - Prevent injury to cornea: eyelid drop; tape eyelid shut. - Antiviral. - Prednisone: must be given within 48-72 hours after onset of symptoms.