Recurrent sigmoid volvulus in a patient with Parkinson’s disease

Clinical Autonomic Research -     

Pisa syndrome in Parkinson’s disease: an electrophysiological and imaging study

The pathophysiology of postural abnormalities in patients with Parkinson’s disease is poorly understood. In the present study, 13 patients with Pisa syndrome (PS) underwent EMG study of paraspinal lumbar (L2–L4) and thoracic (T8–T10) muscles, and of non-paraspinal muscles. Patients also underwent a whole spine X-ray and an MRI assessment of paraspinal muscles (L1–S1). The EMG evaluation disclosed two main patterns: patients with pattern I (n = 6, hyperactivity of lumbar paraspinals ipsilateral to the trunk leaning side) or pattern II (n = 7: hyperactivity of lumbar paraspinals contralateral to the trunk leaning side. In pattern I, half the patients also had ipsilateral hyperactivity of the thoracic paraspinals, the other half had contralateral thoracic hyperactivity; in pattern II, thoracic paraspinal hyperactivity was contralateral in all patients (like the lumbar paraspinal hyperactivity). Non-paraspinal muscles were hyperactive ipsilaterally in four of six patients with pattern I and in all patients with pattern II. The MRI showed mild muscular atrophy with fatty degeneration in patients with pattern I, whereas in pattern II patients this was greater and prevalent on paraspinal lumbar muscles ipsilateral to the leaning side. The present data support the hypothesis that two main patterns of muscular activation are associated with PS. In both patterns, hyperactivity of contralateral paraspinal muscles is probably compensatory for the trunk leaning.     

Impulsive smoking in a patient with Parkinson’s disease treated with dopamine agonists

Impulse control disorders, including pathological gambling, binge eating, compulsive shopping and hypersexual behaviors, have frequently been reported as a side effect of dopaminergic medications for Parkinson’s disease (PD). Here we describe a patient with PD who developed an unusual manifestation of impulsive behaviors, including cigarette smoking, associated with an increase in dopamine agonist medication. We postulate this to be related to an overstimulation of mesolimbic dopamine receptors responsible for reward-seeking behaviors. Further research is needed to examine impulsive cigarette smoking in PD.     

Non-dopaminergic therapy in Parkinson’s disease

Parkinson’s disease no longer seems to be a disease entity caused by only one pathogenetic factor. The facile characterization of Parkinson’s disease as a more or less isolated disorder of the dopaminergic system proves to be an unacceptable oversimplification of the pathology of the disease. Characteristically, not all dopaminergic systems of the central nervous system are involved in the degenerative process. In addition to the nigrostriatal dopaminergic pathway, parts of the glutamatergic, cholinergic, tryptaminergic, noradrenergic, adrenergic, serotonergic, and peptidergic neurons show serious cytoskeletal damage. In the light of these findings, drugs influencing these transmitter systems should be useful in the treatment of parkinsonian symptoms. For this reason, non-dopaminergic drugs are gaining more and more importance. Besides the theoretically interesting adenosine A2 receptor antagonists, budipine, a polyvalent potent new antiparkinsonian drug, has been tested in clinical studies. Budipine is a potent non-dopaminergic antiparkinsonian drug with pharmacological effects that are not comparable to those of conventional drugs applied in Parkinsonian pharmacotherapy. Budipine experimentally increased the brain content of noradrenaline, dopamine, serotonin, and histamine. The dopamine, serotonin, noradrenaline, gamma aminobutyric acid (GABA), and endorphine receptor affinities were not altered, but N-methyl-D-aspartate (NMDA) and sigma receptor affinities were increased as shown by in vivo and in vitro trials with budipine. MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and MPP⁺ antagonistic effects have also been demonstrated. Budipine also shows neuroprotective as well as symptomatic antiparkinsonian effects. In two randomized, double-blind, multicenter, placebo-controlled studies, relevant therapeutic effects have been observed in previously untreated, so-called “de-novo” parkinsonian patients and in subjects in later stages of the disease. Budipine significantly reduces akinesia, rigidity, and tremor. Optimal effects of budipine can be seen 4–6 weeks after starting treatment with this substance. Budipine can be added to all available antiparkinsonian drugs. An open, prospective, long-term study of 2532 patients with Parkinson’s disease (Study BY701/01A) confirmed the favorable safety and tolerability profiles of budipine.

     

Pramipexole-related chronic lower limb oedema in a patient with Parkinson’s disease

Pramipexole is a non-ergot dopamine agonist that is used frequently as a single therapy or in combination for the management of Parkinson’s disease. Common side effects are daytime drowsiness, hypotension, hallucinations and compulsive behaviour. We describe a patient who developed severe chronic and extensive lymphoedema after pramipexole was introduced and that resolved after its cessation.     

Smoking-induced transient motor deterioration in a levodopa-treated patient with Parkinson’s disease

We report a 53-year-old patient with Parkinson’s disease who complained of transient worsening of motor symptoms after smoking a tobacco cigarette. She had been a chronic smoker of one packet of cigarettes a day for over 20?years. We objectively assessed her motor performance including repetitive finger tapping (RFT) speed using 3D kinematic recordings, timed finger tapping test (TFT) and Unified Parkinson’s Disease Rating Scale (UPDRS) III before and after the administration of nicotine, and with and without levodopa. Nicotine was delivered by either smoking a cigarette or by intranasal nicotine spray. Without levodopa, acute deterioration in RFT speed was observed 10?min after both routes of nicotine administration. With levodopa, there was acute deterioration in RFT speed after smoking cigarette, followed by a delayed rebound improvement. However, the administration of nicotine spray led to immediate and sustained motor improvement without initial deterioration. UPDRS III and TFT showed similar trends of acute motor deterioration after either smoking or use of the spray without intake of levodopa. Transient motor worsening after smoking tobacco has been previously reported in only one patient with Parkinson’s disease. The objective findings of acute motor deterioration following both cigarette smoking and nicotine spray administration suggest that nicotine might be the cause of the negative motor effects in this patient. Similar changes were not observed after the administration of placebo intranasal spray. At low dose or beginning of dose, nicotine induces sub-threshold stimulation of dopamine release, which selectively activates the pre-synaptic D2 autoreceptors, leading to transient motor worsening. The potential mechanisms of the additive effect of levodopa and nicotine and paradoxical motor improvement after administration of high-dose nicotine via intranasal nicotine spray are also discussed.     

Switch from selegiline to rasagiline is beneficial in patients with Parkinson’s disease

The objective of this study is to demonstrate that application of rasagiline instead of selegiline with concomitant determination of l-amphetamine and l-methamphetamine in plasma is safe and well tolerated and influences sleep, mood, and motor behavior in patients with Parkinson’s disease on a stable drug therapy. 30 patients, who took 7.5 mg selegiline daily for at least 3 months, were switched to 1 mg rasagiline. Then they were followed over an interval of 4 months. The remaining drug therapy remained stable. This changeover was safe and well tolerated. l-Amphetamine and l-methamphetamine only appeared during selegiline treatment. Motor behavior, motor complications, mood and sleep improved during rasagiline administration. Amphetamine-like derivatives of selegiline could contribute to sleep disturbances, which may be involved in worsening of mood. Motor behavior and motor complications probably became better due to the additional glutamate receptor antagonizing properties of rasagiline in this open label study.     

Secondary failure after ten years of pallidal neurostimulation in a patient with advanced Parkinson’s disease

Deep-brain stimulation of the subthalamic nucleus and internal globus pallidus are both surgical options in advanced Parkinson’s disease. The best target is still debated with data suggesting better motor outcome in subthalamic stimulation but higher rates of psychiatric problems. Failure of pallidal stimulation within the first 2 years has been described. Here, we report a patient with good response to pallidal neurostimulation who developed a secondary failure after 10 years of treatment which was successfully reversed by reimplanting the electrodes into the subthalamic nucleus. This case suggests that a controlled comparison of treatment efficacy of pallidal and subthalamic neurostimulation may require a very long follow-up period to yield reliable results.     

Dyskinesia-hyperpyrexia syndrome in Parkinson’s disease: a systematic review

Clinical Autonomic Research - Dyskinesia-hyperpyrexia syndrome (DHS) is a rare but life-threatening disease. The clinical manifestations of this syndrome overlap substantially with Parkinson...     

Hypoglycemia-induced hemichorea in a patient with Fahr’s syndrome

Non-ketotic hyperglycemia may be a cause of hemiballism-hemichorea. We present an elderly female type II diabetic patient with right-sided hemiballism-hemichorea of acute onset during hypoglycemia following insulin overtreatment of non-ketotic hyperglycemia. Brain computerized tomography and magnetic resonance imaging scans revealed characteristic hyperdensity and T1 hyperintensity, respectively, in the left basal ganglia, in addition to pallido-dentate calcifications, suggestive of Fahr’s syndrome. Although extremely rare, hypoglycemia may be a cause of hemiballism-hemichorea especially in the presence of predisposing factors such as previous hyperglycemic episodes and Fahr’s syndrome.     

Rhabdomyolysis induced by severe levodopa induced dyskinesia in a patient with Parkinson’s disease

Journal of Neurology -     

Rapid onset of efficacy of rasagiline in early Parkinson’s disease

Rasagiline is a monoamine oxidase type-B inhibitor used as monotherapy or in addition to levodopa in the treatment of Parkinson’s disease (PD). This naturalistic single-blind study was aimed at evaluating the rapidity of onset effect of rasagiline on motor symptoms in a cohort of early relatively elderly PD patients. 102 outpatients (55 males, median age 71 years) have been selected: 26 were PD therapy-naive and 76 received rasagiline as add-on therapy. The third section of the Unified Parkinson’s Disease Rating Scale (UPDRSIII) and the Hoehn–Yahr (HY) scale were assessed at baseline and after 1 and 4 weeks thereafter. The mean UPDRS III total score (?6.7 at week 1 and ?8.9 at week 4) and single items, as well as mean HY score (?0.40 at week 1 and ?0.67 at week 4), significantly decreased from baseline (p < 0.001). Improvements were significant in both therapy-naive and add-on therapy patients: the mean decreases from baseline to week 4 in UPDRSIII and HY score were ?8.8 and ?0.46, and ?9.0 and ?0.74, respectively, in the two subgroups. The mean decrease from baseline in UPDRSIII and HY score did not significantly differ in patients aged > or ≤71 years. Rasagiline had a rapid therapeutic effect from the first week of therapy, which further improved at 4 weeks. The rapid onset of action and the absence of a dose titration are important issues in the management of the PD patient.