PARKINSONíS DISEASE

†††† Parkinsonís disease is characterized by a characteristic pill rolling tremor, bradykinesia, mask-like facies with a reduced blinking frequency (hypomimia), simian posture, cogwheel rigidity, gait disturbances, and impaired postural reflexes.† Postural instability is often a late manifestation, and dementia is also frequently encountered in patients with advanced disease.† Other associated symptoms include depression and the restless legs syndrome.† Parkinsonís disease results from a loss of dopaminergic neurons in the substantia nigra, which results in decreased thalamic stimulation of the motor cortex.† A loss of greater than 80% of the dopaminergic neurons occurs before the manifestation of symptoms.† Another associated pathologic finding is the presence of Lewy bodies.† Lewy bodies are small eosinophilic hyaline inclusions which occur in the substantia nigra, locus ceruleus, brain stem, and cerebral cortex.† However, Lewy bodies may be associated with other conditions.† The mean age at time of diagnosis is 55 to 60 years old.† Both underdiagnosis and overdiagnosis are common.† Afflicted patients have a two to five times higher mortality when compared to age matched controls.† A similar parkinsonism syndrome may be seen with other disorders such as drug side effect (Parkinsonism due to neuroleptics or metoclopramide), Wilsonís disease, and neurodegenerative disorders (postencephalitic parkinsonism, posttraumatic parkinsonism, medication/toxin side effect, anoxic brain injury, Alzheimerís disease, Shy-Drager syndrome, normal-pressure hydrocephalus, progressive supranuclear palsy, olivopontocerebellar atophy, Pickís disease, Huntigtonís disease, etc.).

†††† The initial presentation of Parkinsonís disease is varied.† Many patients present with either extremity clumsiness, loss of facial expressions, pill rolling tremor, easy fatigability or nonspecific pain.† A decreased sense of smell may also be the sole presenting symptom.† At disease onset, most symptoms are unilateral or asymmetric.† Patients often relate difficulty with dressing themselves (family members will relate that this activity has become protracted) or complain of feeling stiff.

†††† Classic symptoms are elicited on physical examination.† First notice the patientís posture in the standing position.† Flexion of the upper extremities, upper trunk and head are noted in patients with a simian posture.† A resting pill rolling tremor is often noted.† The tremor is often noted early in disease onset and is often unilateral at first.† It is important to distinguish the pill rolling tremor from essential tremor.† The difference being that essential tremor is generally a postural tremor and is faster than the characteristic parkinson tremor.† Cogwheel rigidity will be appreciated with passive movement of the patients limb.† This may be done by grasping the patients hand as in a hand shake and then rotating the forearm in a circular motion while stabilizing the upper arm by grasping the patientís elbow with the examiners other hand.† Cogwheel rigidity manifests as a ratchet like movement of the lower arm when this test is performed.† Impaired postural reflexes are noted by pushing on the patients chest with a mild quick thrust.† Patients without parkinsons should be able to compensate and maintain their balance whereas patients with parkinsons will not be able to compensate and will lose their balance.† It is important to warn patients that you are going to perform this test and that they should try to maintain their balance.† It is especially important to stand behind the patient in case they should fall backwards so that the examiner can catch the patient and prevent a fall.† A sample of the patientís writing should be obtained and examined for micrographia (small print) which is often noted in patients with parkinsonís disease.† The diagnosis is made clinically when patients manifest some or all of these symptoms, and is often confirmed by noting an improvement in the patientís symptoms in response to a trial of therapy with carbidopa/levadopa.

†††† Medical therapy is varied and includes carbidopa/levadopa combination products (consider another diagnosis in patients who do not respond to this therapy), dopamine agonists (bromocriptine mesylate, pergolide mesylate, pramipexole, and ropinirole HCl), selegiline HCl, rasagiline, amantidine HCl, anticholinergics (trihexyphenidyl and benztropine mesylate), and COMT (catechol-O-methyltransferase) inhibitors (entacapone and tolcapone).† Dopamine agonists are often used for early mild disease with carbidopa/levadopa added later as symptoms progress.† As the disease progresses, symptoms become more severe and difficult to control; therefore, consultation with a neurologist skilled in treating parkinsonís disease may be prudent.† Some cases may warrant surgical intervention.† Current surgical options include pallidotomy, thalamotomy, subthalamotomy, deep brain stimulation of the pallidum, subthalamic nucleus or ventral intermediate nucleus of the thalamus.

†††† Psychiatric complications of Parkinsonís disease include hallucinations and psychosis.† Therapeutic options include clozapine (25-50 mg/day), quetiapine (12.5-75 mg/day), risperidone and ziprasidone.† The dosages used are extremely low but are effective in Parkinsonís patients and help avoid side effects.† Depression is also common in these patients and responds well to typical antidepressants.