Just because you may be plagued by one illness, does not exempt you from acquiring another. So it is that 5% of patients with HIV contract symptoms of Parkinson's disease. Whether due to exposure of typical things like pesticides, well- water, or heavy metals, or because an HIV patient may have prior exposure to neuroleptic medications and opportunistic infections, it is unclear how and whether one illness relates to the other. Parkinsonism has also been reported as the presenting symptom of HIV. In a recent issue of the journal, Movement Disorders a healthcare team from the Salford Royal Hospital, UK reported on a patient with HIV who received a diagnosis of idiopathic Parkinson's disease and suffered from dyskinesia. The patient underwent treatment with highly- active antiretroviral therapy and experienced resolution of the parkinsonian symptoms.

In 2001, the patient was a 40- year old homosexual man in a relationship, with no history of injectable drug use or foreign travel. He described a three-year history of parkinsonism on one side of the body.  He reported having difficulty writing and noticed the loss of manual dexterity due to tremor in the left hand. Examination noted the presence of seborrhoeic dermatitis of the face. He had signs of upper and lower limb resting and postural tremor, though slowness of movement and rigidity were confined to the left side of the body. He had full facial expression, and no problems with eye movements.

Symptoms of right- sided illness and compromised balance were apparent approximately a year later. A clinician recommended dividing the 800 mg/ day of levodopa into smaller doses. The amendment made some improvement, though marked motor fluctuations, and dyskinesia appeared within six months. The patient began taking amantadine along with continuous subcutaneous apomorphine infusion. The method of delivering medication to the body allowed a reduction in levodopa to 300 mg/day and mildly improved motor complications.

In 2004, the patient underwent an excisional biopsy of the parotid glands due to bilateral swelling. Results showed benign cystic changes in cells. An HIV test came back positive. Other testing provided a CD4 count of 150 (normal for HIV+ is 500) and a viral load of >750,000 (the very upper limit). Neuropsychological testing showed mild impairment of short- term memory. The patient began highly- active anti-retroviral therapy: lamivudine/ zidovudine and lopinavir/ ritonavir with a marked reduction in his viral load. Symptoms of parkinsonism improved over the following months allowing him to discontinue the apomorphine infusion, and gradually withdraw from levodopa. In a follow- up appointment in April 2008, the patient exhibited no resting tremor or bradykinesia. Rigidity was absent at rest and with co-activation.

HIV- infected patients with increased cell loss in the substantia nigra have been described, though these patients have been free of neurological abnormalities. PET studies have shown increased metabolism levels in the basal ganglia in early HIV infection, with reduced metabolism occurring in advanced illness. The authors concede the abnormalities they describe in the patient could be explained by reversible dopaminergic dysfunction secondary to HIV infection; though the span of time the patient suffered from symptoms, seems exceedingly long. They advocate HIV should remain in the differential diagnosis of young- onset PD, given its potential resolution by highly active anti- retroviral therapy.

Kobylecki C. et al. Letter to Editor HIV- associated parkinsonism with levodopa- induced dyskinesia and response to highly- active antiretroviral therapy. Movemnt. Dis. Early view  11 Nov. 2009.

Journals publish letters sent to their editors to enlighten clinicians, students and others about unusual patient cases. The following story describes an atypical response to the medication, rasagiline. Prescribed for patients with PD, it is thought to harbor neuro- protective effects.

The sixty- five year old patient was born with spina bifida, but had no dysfunction of bowel, bladder, or sexual function. The patient received a diagnosis of PD at age sixty- one and took 2mg rasagiline to treat his symptoms.  A month after initiating treatment with levodopa he experienced spontaneous ejaculation occurring in clusters, every ten minutes for thirty minutes. Such episodes happened every two to seven days. Ejaculation took place without an erection and with no stimulation. In between these episodes he had regular sexual activity with no autonomic problems.

On his neurological exam, the clinician found left- sided rigidity, and slowness of movement without a resting tremor. The dorsiflexors were mildly weak, and he had decreased proprioception of vibration in the toes of both feet. The lower body had decreased reflexes.

The episodes of spontaneous ejaculation continued even when the dose of rasagiline dropped by half, but stopped when he discontinued the drug. Without rasagiline, the patient noted his symptoms worsened, and his clinician subsequently prescribed a four-month course of 10 mg of selegiline daily, to counteract additional movement concerns. After a period of four months, without sexual side effects, the patient began rasagiline anew, at 2 mg per day. Within a month spontaneous ejaculations re-occurred. The patient elected to stay on the medication, and still experiences unprompted orgasms. He also noted orgasms associated with planned sexual activity are more explosive, with less recovery time needed between such events.

Apart from hypersexuality, the prevalence and range of sexual dysfunction in those with PD, gets little attention. However, numerous reports of sexual problems occurring after the use of dopamine agonists, specifically apomorphine and ropinirole exist. This report, the authors believe, is the first of its kind.

Researchers noted dopamine's role in inducing an erection when apomorphine was undergoing drug trials for the treatment of alcoholism. Apomorphine is a powerful dopamine receptor agonist and has been marketed as a treatment for human erectile dysfunction. Bromocriptine and ropinirole, two other dopamine agonists are reported to have improved erectile dysfunction, as well.

Experiencing ejaculation without an erection is curious. The author notes animal studies have shown dopamine aids ejaculation. For ejaculation to occur without an erection, different dopamine receptor sub types may come into play, as stimulation of D2 receptors in the rat's pre- optic area by the D2/D3 receptor agonist, quinelorane, promotes ejaculation. Piribedil, another D2 and D3 receptor agonist significantly increases rat ejaculation with less effect on erection. Further support that D3 receptors in the brain modulate orgasm and the period between ejaculations, appeared when technicians injected a selective D3 receptor antagonist into the medial pre- optic area of the rat brain, abolishing ejaculations without affecting erections. It is also possible rasagiline increases central dopamine at either the brainstem or medial pre- optic area to increase signals to the spinal cord ejaculation center. The author concedes the patient is unique due to his underlying spina bifida, suggesting spinal cord or peripheral involvement is responsible for the aberrant reaction to rasagiline. As neurologists inquire more frequently into the sexual function of their patients, and with increasing use of rasagiline, more instances of the unusual side effect should occur.

A patient arrived for the first time at clinic today with striking symptoms of Parkinson's disease. A very detailed history of when the first signs occurred followed, with acute insight into what presented and how the initial feeling of pain in one arm got interpreted as a muscle strain. After noticing the pain persisted throughout the day, for several days, then months the patient noted decreased strength in the arm. Objects once easily manipulated spilled onto the kitchen floor.

The patient lay on the bed at night wondering whether the spouse would notice the bed shaking. The inner tremor continued as did the pain in the arm. The specialist comments that studies have been done on patients who feel an inner sense of tremor, and that the symptom, once thought to correlate with anxiety, was shown to correspond with depression.

The patient nods in understanding and seeks to relate more of the history; bringing a foot into the air as one does in ascending a step, has become problematic.  In order to perform the feat, the patient is forced to hang on to the railing. Akin to this issue, is the inability to rise from a chair without using the arms. In eating lunch, the patient finds his arm has lost the fluidity of movement it had. It is almost as though the arm and hand holding the fork, move in ratchet-like motion.

The physician states two over -the- counter measures may be useful are coenzyme Co Q10 at 900-1200 mg/day and creatine at 20 grams/day. The two have been found to improve mitochondrial function. The doctor comments the autonomic nervous system becomes involved in PD, and patients typically find themselves contending with constipation. The patient nods in agreement, relating some relief of the symptom through a remedy by Planetary Herbal Formulas, something called Triphala. Frequent urination is another symptom the patient notes, occurring at night. The doctor responds that many patients comment on this.

The patient concedes that the weight loss through healthy eating of many fruits, vegetable and whole grains was intended, thirty three pounds came off rather easily in the last year. The physician asks the patient to move to the examination table. While moving, the patient clasps every stable surface on the way to the exam table. The physician asks to see the patient walk, and the feet appear to be magnetically fastened to the floor. The patient has no arm swing. To gauge the ability to recover from a perturbation in balance, the physician cues the patient about what he plans to do, then jostles the patient's shoulders. The patient throws the arms wide and has extreme difficulty righting the torso under the feet. Problems with recovering from a balance disturbance typically present themselves in Stage III illness.

Back in the confines of the small office, the specialist explains that when a patient's signs or symptoms create impairments that conflict with working, or performing routine activities, he prescribes medications to dampen symptoms of PD. Most drugs have secondary affects. Though both creatine and Co-Q10 will do nothing to quiet the issues, they may delay the worst of the illness. Rasagaline, or Azilect is a prescription medication proven to delay the need for levodopa in PD patients. An MAO inhibitor, it carries a black- box warning because it may bring on a hypertensive crisis when combined with red wine and aged cheeses.

The patient stretches an arm over the notes the physician provides, and divulges that rather than taking the drugs more time needs to be given to an alternative method. The medications will be there, available when hope runs out that other means may alleviate the most troubling symptoms. Yes, the physician agrees, this is a patient decision; yet he wants the patient to return in four months to check on progress.