The familial incidence of benign paroxysmal positional vertigo.

The goal of this investigation was to determine whether there is a familial tendency in the development of benign paroxysmal positional vertigo (BPPV). We hypothesized an increased frequency of BPPV among relatives of patients with the same diagnosis. BPPV is caused by dislodged otoconia from the utricular macula floating in the semicircular canals. At least half of BPPV cases are idiopathic and most pathological associations provide no clue as to the reason otoconia become dislodged. We have noted a number of BPPV patients with family histories of BPPV, suggesting a genetic predisposition to the condition. We surveyed 120 successive BPPV patients and 120 successive dizzy patients without BPPV regarding the frequency of dizziness and BPPV (diagnosed by a physician) among family members. Patients in our group with BPPV were 5 times as likely to have relatives with BPPV compared to the dizzy control group (chi2=5.95, DF=1, p=0.015). We have demonstrated that there is a familial tendency for the occurrence of BPPV. There is nothing in our data that would distinguish between a hereditary or environmental influence in the development of the disease, however.

Occult anticonvulsant osteomalacia in North India.

Serum calcium, inorganic phosphate and alkaline phosphatase, tubular reabsorption of phosphate (TRP) estimation and radiological examination of the skeleton were conducted in 40 cases (18-50 years of age) on anticonvulsant therapy and 20 controls. The epileptic group showed a statistically significant rise in serum alkaline phosphatase and a fall in TRP. In none of the cases, however, was there clinical or radiological evidence of osteomalacia. Biochemical abnormalities were seen mainly in the youngest individuals. It seems that the critical factor for the development of anticonvulsant osteomalacia is the lack of dietary vitamin D/solar exposure or increased body requirement of the vitamin.