A review of the literature points to the many causes of arachnoiditis and the failure of treatment to arrest or reverse its effects. The true incidence cannot be determined, although it is probably lower than might at first appear from the published articles. In the radiological literature the diagnosis seems to derive from an examination of the films alone, often without reference to the clinical findings or appearance at operation. While attempts at treatment are usually unsuccessful, some iatrogenic cases can be prevented by the avoidance of intrathecal steroid injections or unduly rough or repeated surgical exploration of the lumbar vertebral canal.

Since the introduction of levodopa therapy, there have been major advances in the understanding and treatment of Parkinson’s disease. However, the problems and limitations associated with this form of treatment are now becoming increasingly apparent. This article reviews some of the current knowledge concerning the etiology and pathophysiology of Parkinson’s disease and discusses some-practical approaches to drug therapy.

To evaluate the usefulness of CT in detecting unexpected brain lesions in epileptics, scan results were analyzed in a consecutive series of 196 adult epileptics in whom there was no known etiology for their seizures nor any abnormality on neurological examination. Nineteen additional epileptics, selected on the basis of an unexpected positive CT were also included for analysis.

In the consecutive series, the overall incidence of abnormal scans was 16% with the highest yield (44%) found in patients with partial elementary seizures. Partial seizures secondarily generalized were correlated with a significantly higher CT positivity than purely partial seizures. Patients with seizures for less than six months more frequently showed CT abnormalities than patients with a longer history.

In 25 of 51 cases with abnormal scans a specific lesion amenable to therapy was detected, including 16 neoplasms and 5 arteriovenous malformations. Other lesions included generalized or focal atrophy, infarcts, calcified lesions of tuberous sclerosis, unexplained calcifications and focal low-density or enhancing lesions.

Chronic subdural hematomas in adults are not technically difficult to treat. They probably constitute one of the most common potentially curable lesions with which the average neurosurgeon deals. Despite this (or perhaps because of it) numerous treatments, radically differing from one another, have been advocated. Fine judgement is called for in deciding whether or not to operate in the first instance, make a flap or one or more burr or twist drill holes, use a drain, employ suction, inflate the brain, leave the bone flap out. In a personal series of 71 chronic subdural hematomas, 46 were treated with a red rubber catheter drain through a burr hole and 23 with a closed system suction drain. The results of this series suggest that closed system suction drainage through a single burr hole is the better of the two techniques. It has important theoretical advantages and the procedure is simple and fast. The complication rate is low and patients have a shortened postoperative hospital stay.

Using medical files, death certificates and an interview at home for the survivors, a long term retrospective follow-up study was done for 82 subjects operated for carotid stenosis. Causes of death, survival rates and medical history of survivors were studied. Subjects were classified in two preoperative risk categories according to their medical history prior to angiography: low risk (36 subjects) and medium risk (46 subjects). None of the subjects were lost during the follow-up period which varies from 81 to 105 months.

At seven years, observed survival rate is significantly lower for the medium risk patients than for the low risk patients (43.0 ±8.6 versus 80.6 ± 6.6; X2 M-H, p = 0.006). The difference between the survival rates is markedly noticeable after the fifth year of follow-up. Besides, the percentage of survivors who have developed cerebrovascular problems after the operation is significantly higher in the medium risk group than the low risk group (54.5% versus 25.0%, X2 p ≃ 0,04).

Does this mean that the preoperative risk classification separates two different stages or two different forms of atherosclerosis? Can. J. Neurol. Sci. 1983; 10:27–31

A case of presumed anticoagulant induced hemorrhage into infarction is presented along with a retrospective study of 110 cases of cerebral embolus.

An accurate recommendation for the timing of anticoagulation following cerebral embolism hinges on balancing the risk of hemorrhage into infarction against the benefits of early treatment attributed to preventing recurrent embolism. It is felt that the present literature, concepts of pathogenesis and experimental data provide insufficient information to make absolute clinical decisions. The available evidence implies that the risk of further embolic events is three to four times that of hemorrhage into infarction, yet additional randomized prospective studies and better experimental models are needed to establish a valid treatment plan. It may be possible to distinguish separate mechanisms underlying early diffuse hemorrhage into infarction from sudden delayed massive hematoma formation.

In a recent paper (Barbeau and Pourcher, 1982) we demonstrated that so-called “idiopathic” Parkinson’s disease is not a homogeneous entity, and defined the existence of a sub-group of patients with genetic parkinsonism. To investigate this last possibility, and to uncover possible metabolic clues as to the etiology of such cases, we carried out a prospective study of 50 kindreds with “familial” parkinsonism. Two control groups were similarly studied: 50 kindreds with essential tremor (neurological control group) and 50 kindreds originating from spouses of the previous patients (non neurological control group). We uncovered two main patterns of genetic transmission within the parkinsonian patients: a parkinsonism related to dominant essential tremor (34 kindreds; 10% of all Parkinsonians) and a recessive “akineto-rigid syndrome” (10 kindreds; 3–4% of all Parkinsonians). A further 4 kindreds assumed a pseudo-dominant pattern but were probably recessive. Finally 2 kindreds were obviously other entities presenting as “phenocopies” of Parkinson’s disease. Metabolically, hyperthyroidism appeared to be more frequent in essential tremor and “essential-tremor related parkinsonism” kindreds, while hypothyroidism and possibly hypoparathyroidism (post surgery) seemed more frequent in the recessive akineto-rigid syndrome kindreds.

Determinations of CSF HVA before and after Probenecid administration were made in 41 patients with Parkinson’s disease. The means of HVA concentration were lower than those of controls but no correlation with clinical data was found. A negative correlation was demonstrated between post-probenecid HVA levels and subsequent score improvement with L-DOPA at 3,6 and 12 months. Post-probenecid HVA levels suggest that there are distinct forms of parkinsonism and could predict the response to L-DOPA therapy.

Different groups of rats were maintained on choline-deprived (CD), choline-supplemented (CS) or standard rat chow diets beginning at a body weight of approximately 100 g, and electrically kindled in the amygdala beginning not less than 40 days later. The CS group kindled significantly faster than the CD group, whereas the CD and chow-fed groups did not differ in their rate of kindling. This result is consistent with both the known effects of the dietary manipulation of choline on brain acetylcholine level, and the idea that acetylcholine has a role in amygdaloid kindling.

In a retrospective study of 4,294 consecutive postmortem cases, there were 15 with histologically proved sarcoidosis, including 4 with CNS involvement. Whereas in previously reported autopsy series the prevalence of neurosarcoidosis was 15%, it is 27% in this review. Five cases with incidental, clinically inapparent sarcoidosis died at a mean age of 54.6 years; those six with systemic sarcoidosis, not involving the CNS, died at a mean age of 47.0 years; while those four with a variety of neurologic manifestations in addition to systemic sarcoidosis died at a mean age of 38.2 years. Thus, it appears that at one end of the spectrum of morbidity, sarcoidosis may cause no or only trivial symptoms and permit prolonged survival. At the other extreme, sarcoidosis may affect a younger population more severely. CNS involvement occurs relatively early in the course and is rather rapidly progressive, accounting for the poor prognosis, despite appropriate medical and neurosurgical management. In its turn, neurosarcoidosis may present with a variety of signs and symptoms, depending on the site of involvement along the craniospinal axis. This feature is illustrated by the manifestations of compression myelopathy, hydrocephalus with dementia, hydrocephalus with seizures and ataxia, and anosmia, blindness, seizures, and diabetes insipidus. In addition, one patient developed a Nocardia brain abscess as a complication of the altered immune system in sarcoidosis.

A 33 year old man developed bilateral leg weakness two years following radiotherapy to the pelvis and lower abdomen for the treatment of a seminoma. Clinical and electrophysiological examinations and nerve and muscle biopsies suggest that this is an example of either post-irradiation myelopathy selectively affecting the anterior horn cells in the lower spinal cord or a purely motor lumbo-sacral radiculopathy.

A case of tuberous sclerosis diagnosed at autopsy in a neonate at 28 weeks gestation is described. This is believed to be the earliest case yet reported. The CNS lesions consist of cortical tuberosities, heterotopic white matter nodules and subependymal nodules. These nodules consist predominantly of giant astrocytes but a small undifferentiated cell component is present as well. Multiple cardiac rhabdomyomas are also present. An explanation for neuronal hypocellularity within the cortical tuberosities is suggested.

Two patients with acute hemorrhagic leukoencephalopathy, one of which was pathologically proven, were serially studied with CT scanning. Both patients showed marked distinctive low density white matter changes throughout both hemispheres, which correlated with clinically involved areas. One patient recovered from the disease, perhaps due to steroid treatment, and showed slow but complete resolution of CT scan changes. We feel that CT scan findings significantly help in the diagnosis of this disease, which may be amenable to early treatment with steroids.