Pseudorandom binary sequence stimulation applied to the visual evoked response. Normative data and a comparative study with pattern and flash stimulation.

The investigation of patients who are unable to fixate the pattern visual stimulus generally requires the use of diffuse flash stimulation to elicit the visual evoked response. However, by comparison with pattern, flash stimulation has proved relatively insensitive in identifying lesions of the visual pathway. We investigated a more complex method of flash stimulation. A pseudorandom binary sequence has been used to generate the diffuse visual evoked response stimulus. The pseudorandom binary sequence, rather than producing a single flash, switches in a pseudorandom fashion between two levels of illumination. The result is a diffuse visual stimulus approximating band-limited white noise. The series is periodic, enabling signal averaging to be performed. By applying the methods of random signal analysis, the impulse or transient response of the visual pathway can be determined. Our normal pseudo-random binary sequence visual evoked response impulse function, derived from 29 normal subjects, had the morphologic characteristics of the conventional flash visual evoked response and a major positive component (P100), whose latency mean and standard deviation closely matched that of our normative pattern visual evoked response. However, the P100 amplitude standard deviation was significantly greater than that produced by conventional pattern and flash stimulation. We investigated 140 patients by means of pattern, flash and pseudorandom binary sequence stimulation. The pseudorandom binary sequence visual evoked response proved to be almost 12 times more effective than flash visual evoked response in detecting lesions of the visual system.

Vascular changes in leprosy and its role in the pathogenesis of leprous neuritis.

The arteriographic pattern of left hand vessels was studied in 20 patients in leprosy by percutaneous brachial arteriography. Arteriographic abnormalities noted consisted of occlusion, narrowing, tortuosity, dilatation, irregularity and incomplete filling of the lumen by contrast medium. Such abnormal findings were seen in all the arteriograms studied and more than one vessel involvement was noted in over 50 percent cases. This study clearly demonstrated that arterial involvement in leprosy was frequent. No correlation was found between motor weakness and vascular abnormalities. There was no difference in arterial lesions between the patients with and without trophic changes. There was also no correlation between the severity of vascular changes and decline in motor nerve conduction. Degree of histopathological abnormalities in the sural nerve biopsy from these patients showed no features of micro angiopathic neuropathy. It is concluded that the observed vascular abnormalities do not contribute significantly in the genesis of neurological deficit in leprosy.

Vascular changes in leprosy and its role in the pathogenesis of leprous neuritis

The arteriographic pattern of left hand vessels was studied in 20 patients in leprosy by percutaneous brachial arteriography. Arteriographic abnormalities noted consisted of occlusion, narrowing, tortuosity, dilatation, irregularity and incomplete filling of the lumen by contrast medium. Such abnormal findings were seen in all the arteriograms studied and more than one vessel involvement was noted in over 50 percent cases. This study clearly demonstrated that arterial involvement in leprosy was frequent. No correlation was found between motor weakness and vascular abnormalities. There was no difference in arterial lesions between the patients with and without trophic changes. There was also no correlation between the severity of vascular changes and decline in motor nerve conduction. Degree of histopathological abnormalities in the sural nerve biopsy from these patients showed no features of micro angiopathic neuropathy. It is concluded that the observed vascular abnormalities do not contribute significantly in the genesis of neurological deficit in leprosy.

Multiple sclerosis in North-West India.

Fifty-four patients, with multiple sclerosis from North-West India are described. This included two pathologically proven cases of multiple sclerosis. Five patients conformed to the definition of neuromyelitis optica (Devic's syndrome). This study is in agreement with the other series reported from Asia regarding the special clinical features of multiple sclerosis described from this part of the world. There is more common occurrence of visual impairment at onset, predominant involvement of optic nerves and spinal cord and higher incidence of classical neuromyelitis optica. There is no relationship of any or all cerebro spinal fluid abnormalities with the type of multiple sclerosis, duration of an attack and disability, except for the possible relation between the type of colloidal gold reaction pattern and the type of multiple sclerosis.

Role of porta systemic shunt and hepatocellular damage in the genesis of hepatic neuropathy.

A study was undertaken to evaluate the relative role of porta-systemic shunts and hepatocellular damage in the genesis of neuropathy in chronic liver disease. Two of the 14 patients with non-alcoholic cirrhosis showed clinical evidence of neuropathy, whereas none of the patients with idiopathic portal fibrosis had evidence of neuropathy clinically. Decreased motor conduction velocities were present in some cases of idiopathic portal fibrosis as well as non-alcoholic cirrhosis. Subclinical evidence of histopathological neuropathy in the form of segmental demyelination and remyelination as well as myelin fiber loss was seen in 10 out of 11 sural nerves studied in idiopathic portal fibrosis group and in all the 10 patients in the non-alcoholic cirrhosis group. No correlation was found between histological features and various parameters studied. It is postulated that the development of clinical or subclinical neuropathy in chronic liver disease depends on two factors, being collateral shunting and hepatocellular damage or both and probably related to abnormalities of nitrogen metabolism.

Pathology and time relationship of peripheral nerve changes in experimental diabetes.

Structural changes have been studied in peripheral nerves in streptozotocin-induced diabetic monkeys. Teased single nerve fibre preparations were most informative. Abnormalities were present in 32 of 58 nerves examined from 15 diabetic monkeys with varying degree of hyperglycaemia. The earliest change was an increase in the gap at nodes of Ranvier, seen 12 weeks after the diabetic state had been established. Well marked segmental demyelination was seen in distal nerves at 14-16 weeks. Later similar changes were seen in proximal, larger nerves. Evidence of remyelination was present at a later date. Wallerian degneration was seen in only 4 nerves. Changes in the myelin sheath were more prominant than axonal abnormalities at all times. There was no abnormality in the vasa nervorum and only a mild increase in endoneurial and perineurial fibrous tissue. A direct correlation was present between the extent and degree of pathology and both severity as well as duration of hyperglycaemia.

Pseudohypertrophic myopathy in cysticerosis.

A patient with diffuse involvement of the central nervous system and pseudohypertrophic muscular changes induced by cysticerci is described. Electromyographic and pathologic changes are reported for the first time. Electromyographic examination demonstrated numerous short-duration, low-amplitude motor unit potentials in proximal muscles. Biopsy showed swelling of muscle fibers, fiber atrophy with fibrosis, and cellular infiltration separate from inflammatory exudate surrounding numerous cysts.