Simultaneous bilateral ulnar neuropathy: an unusual complication caused by neuroleptic treatment-induced tardive dyskinesia: A Case Report.

RATIONALE: In the past decade, only a few studies have focused on simultaneous bilateral ulnar neuropathy. PATIENT CONCERNS: A 54-year-old Asian male who has suffered from paranoid schizophrenia for 2 years. He reported that flexion contracture occurring over his fourth and fifth fingers on both hands appeared since six months after he started taking the antipsychotic drug. The electromyogram revealed bilateral ulnar neuropathy with chronic axonal degeneration at the elbow level. McGowan classification was performed to evaluate the severity of the ulnar nerve injury, and the patient was diagnosed with a grade 3 injury on his left hand and a grade 2 injury on his right hand. DIAGNOSIS: Simultaneous bilateral ulnar neuropathy at the elbow, a complication caused by tardive dyskinesia in a patient under the high-dose, first-generation, antipsychotic drug. INTERVENTIONS: We consulted a psychiatrist to assist in adjusting the patient's kind of the antipsychotic drug and performed the anterior transposition of ulnar nerve to avoid nerve entrapment caused by tardive dyskinesia. OUTCOMES: Numbness of the palms continued to regress over the following 6 months after the anterior transposition of the ulnar nerve. Regression of the involuntary movements, including repeated bending of the elbows, and shaking of both feet, was noted from the patient but was incomplete. LESSONS: Two literatures concluded that parkinsonian rigidity is the main cause of simultaneous bilateral ulnar neuropathy by Sampath et al and Kurlan et al. Unlike the cases of stereotyped posture-caused neural compression reported previously, we inferred that repeated involuntary motion caused by first-generation antipsychotic drug might have been one of the causes of the patient's nerve compression.

δ-Aminolevulinic acid dehydratase genotype predicts toxic effects of lead on workers' peripheral nervous system.

There is a wide variation in sensitivity to lead (Pb) exposure, which may be due to genetic susceptibility towards Pb. We investigated whether a polymorphism (rs1800435) in the δ-aminolevulinic acid dehydratase (ALAD) gene affected the toxicokinetics and toxicodynamics of Pb. Among 461 Chinese Pb-exposed storage battery and 175 unexposed workers, allele frequencies for the ALAD1 and ALAD2 alleles were 0.968 and 0.032, respectively. The Pb-exposed workers had a higher fraction of the ALAD1-2/2-2 genotype than unexposed workers (7.8% vs. 2.3%, p=0.01). The Pb levels in blood (B-Pb) and urine (U-Pb) were higher in Pb-exposed workers carrying the ALAD2 allele compared to homozygotes for ALAD1 (median B-Pb: 606 vs. 499 µg/L; U-Pb: 233 vs. 164 µg/g creatinine), while there was no statistically significant difference in the unexposed controls (median: 24 vs. 37 µg/L, and 3.9 vs. 6.4µg/g creatinine, respectively). High B-Pb and U-Pb were associated with statistically significantly lower sensory and motor conduction velocities in the median, ulnar and peroneal nerves. At the same B-Pb and U-Pb, ALAD1 homozygotes had lower conduction velocities than the ALAD2 carriers. There were similar trends for toxic effects on haem synthesis (zinc protoporphyrin and haemoglobin in blood) and renal function (albumin and N-acetyl-d-ß-acetylglucosaminidase in urine), but without statistical significance. There was no difference in Pb toxicokinetics and toxicodynamics associated with VDR BsmI polymorphism. Our results show that the ALAD genotype modifies the relationship between Pb and its toxic effects on the peripheral nervous system. This must be considered in the assessment of risks at Pb exposure.

Quantifying deficits in the 3D force capabilities of a digit caused by selective paralysis: application to the thumb with simulated low ulnar nerve palsy.

We present the development of a vision-feedback method to characterize how selective paralysis distorts the three-dimensional (3D) volume representing digit-tip force production capability and its application to healthy individuals producing thumb-tip force with and without simulated low ulnar nerve palsy (LUNP). Subjects produced maximal static voluntary force spanning the transverse, sagittal and frontal planes of the thumb (16, 15 and 10 subjects, respectively). Subjects produced thumb-tip force tasks in guided and self-selected directions. The envelope (convex hull) of extreme forces in each plane approximated that cross-section of the 3D volume of force capability. Some subjects repeated the tasks with a temporary ulnar nerve block applied at the wrist to simulate complete acute LUNP. Three geometric properties of the force convex hull characterized each cross-section's shape: the ratios of its principal moments of inertia (RPMIs), the orientation of its principal axis (OPA), and its centroid location. Our results show that force production in the thumb's sagittal plane may be a reproducible and objective test to grade motor impairment in LUNP: paired t-tests of the larger RPMI in this plane best distinguished the nerve-blocked cases from the control cases in the guided task (p = 0.012), and Discriminant Analysis of the centroid location for the self-selected task in this plane correctly classified 94.7% of subjects into the control and ulnar nerve-blocked groups. We show that our method measures and detects changes in a digit's force production capabilities. Towards a clinical test of motor impairment in LUNP, this biomechanical study dictates which 3D thumb-tip forces to measure (those in the sagittal plane) and how to measure them (using the self-selected task).

Minocycline-associated lupus-like syndrome with ulnar neuropathy and antiphospholipid antibody.

Peripheral neuropathy in association with minocycline-induced lupus-like reaction has not previously been reported. We present a case of probable minocycline-induced lupus associated with antiphospholipid antibodies and an ulnar neuropathy which has slowly improved since the discontinuation of minocycline.