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W Grisold

Publications and source records attributed to W Grisold.

At least 37 records · Page 2Linked to original sources

[Proximal neuropathy of the median nerve].

In a 77 year old man the rare clinical picture of a complete lesion of the median nerve at the upper arm is described. During removal of a "neurinoma" at the upper arm, inadvertedly the general surgeon had also transsected the median nerve. However diagnosis was delayed due to electrodiagnostic tests, which erronously interpreted the volume conduction of the neigbouring nerves as partial function, and later even as improvement of the median nerve function. Clinically he presented with "orators" hand. He was unable to pinch thumb and index finger, Sensory loss was noted at the fingertip 2 and 3, atrophy of the abductor pollicis brevis muscle and trophic skin changes with an ulcer at the tip of the index finger. Nerve revision confirmed the median nerve transsection. Intraoperative nerve stimulation could not elicit distal muscle stimulation. Sural nerve transplant was performed and within one year a positive Tinel sign progressing 20 cm distally to the operation site, without distal motor or sensory changes was observed.

Aged↗

Clinical and pathologic features of focal myositis.

To clarify the nosology of focal myositis (FM), we report the clinical and pathologic features of eight patients presenting with focal enlargement of one muscle. Most patients improved without immunosuppressive therapy, and none developed polymyositis. Pathologic features were those of an inflammatory myopathy, with muscle fiber hypertrophy and moderate to severe inflammation. In most cases, a clustering of tightly packed muscle fibers, enveloped by a thick bundle of fibrosis, was associated with the diagnosis of FM. Immunohistochemistry showed T cell predominance within the interstitial infiltrates in all cases. No evidence of vasculitis was present. Our findings suggest that FM is a benign condition that has certain clinical features separating it from other inflammatory myopathies. Pathologic changes, such as large clusters of nesting muscle fibers surrounded by thick fibrosis, are more characteristic of FM than polymyositis.

Adolescent↗

T cell-mediated paraneoplastic ganglionitis--an autopsy case.

A 57-year-old woman presented with subacute sensory, ataxic neuronopathy. Clinical investigation revealed a right-sided non-small-cell lung cancer. Serum investigation for specific antineuronal antibodies was negative. Histology showed T lymphocytic infiltrates in dorsal root ganglia. The observed histological pattern is similar to that described in antibody-positive cases. Thus, these findings suggest similar pathways in specific antineuronal antibody-negative and -positive cases of paraneoplastic subacute sensory neuronopathy.

Autoantibodies↗

Intraneural nerve metastasis with multiple mononeuropathies.

Although cancer is a frequent condition, neoplastic involvement of the peripheral nervous system is rare. The mechanisms are heterogeneous and include lesions within the cerebrospinal fluid (CSF) space, local invasion (e.g. brachial plexus), compression, rarely direct infiltration, perineurial spread and even rarer intranerval metastasis. A 47-year-old woman had been treated for a carcinoid 10 years earlier and had received axillar irradiation. At presentation she suffered from weakness of the biceps brachii and was experiencing pain radiating from the axilla into the forearm and thumb. MR scans of the brachial plexus were negative and her symptoms were primarily considered to stem from a postradiation brachial plexopathy, Because of increasing pain, the brachial plexus was explored and a metastasis in the left musculocutaneous nerve was resected. Several months later, numbness and pain appeared in the ulnar nerve and another intrafascicular metastasis in the ulnar nerve was discovered. Resection with preservation of remaining fascicles was performed. This rare case report demonstrates that multiple mononeuropathies, resembling multiplex neuropathy, may be caused by intranerval metastasis.

Brachial Plexus Neuropathies↗

Repetitive phrenic nerve stimulation in myasthenia gravis.

OBJECTIVE: In patients with MG it may be difficult to determine whether respiratory insufficiency is due to a defect in neuromuscular transmission. We therefore studied the clinical value of repetitive electrical stimulation of the phrenic nerve. METHODS: Repetitive phrenic nerve stimulation at 3 Hz was performed in 25 patients with MG. We recorded from the ipsilateral hemidiaphragm with surface electrodes before and after exercising the diaphragm for 10 and 90 seconds. The percent decrement of the negative peak (NP) area between the first and the fifth or sixth diaphragmatic compound muscle action potential (DCMAP) was analyzed and results compared with those from 10 healthy individuals. RESULTS: The mean +/- standard deviation percent change of the NP area in healthy individuals was -2.1 +/- 4.2%, with a normal cutoff of > or = 11%. Twelve patients (48%) had an abnormal decrement of DCMAP--9 had a decrement when the diaphragm was rested, 3 only after fatiguing of the diaphragm. The mean percent change in the 12 patients was 20% at rest, -18% after 10 seconds of exercise, and -23% after 90 seconds of exercise-a pattern consistent with MG. Repetitive stimulation of the accessory nerve with recording of the trapezius CMAP (TCMAP) was abnormal in nine patients (36%). The three patients with abnormal decrement of the DCMAP despite normal TCMAP had symptoms of dyspnea. CONCLUSIONS: Repetitive phrenic nerve stimulation studies are a promising tool in the diagnosis of respiratory muscle weakness in MG and should be part of electrophysiologic studies in patients with undiagnosed respiratory failure.

Adult↗

Neuralgic amyotrophy with phrenic nerve involvement.

Phrenic nerve involvement is a rare feature in patients with neuralgic amyotrophy (Parsonage-Turner syndrome). We report four patients who initially presented with severe dyspnea in the absence of lung disease. All patients had a history of infectious disease or surgery and of pain of sudden onset in the shoulder region. Weakness of the proximal arm was observed in only one. Radiographic and pulmonary function studies, phrenic nerve conduction studies, and needle electromyogram (EMG) of the diaphragm documented diaphragmatic paralysis which was unilateral in one patient, bilateral in two patients, and recurrent on alternating sides in another one. Follow-up studies remained abnormal for up to 4 years. Neuralgic amyotrophy with phrenic nerve involvement should be considered in patients presenting with severe, unexplained dyspnea of sudden onset.

Aged↗

Iliac artery aneurysm causing isolated superior gluteal nerve lesion.

Lesions of the superior gluteal nerve (SGN) lead to weakness of hip abduction, manifesting itself as a gait abnormality, with contralateral tilting of the pelvis with each step. Causes are numerous and may occur at different anatomical locations before the nerve enters the suprapiriform foramen, in the foramen itself, or after the nerve has exited the foramen. This case report describes an SGN lesion by a large iliac artery aneurysm in a patient presenting with a gait disorder.

Buttocks↗

Paraneoplastic neuropathy.

Paraneoplastic neuropathies occur in various settings. This article focuses on recent neuroimmunologic findings regarding paraneoplastic neuropathy. Entities such as sensorimotor and sensory neuropathy, sensory neuronopathy; motor, autonomic, demyelinating and vasculitic mononeuropathies; and cranial nerve lesions and neuropathies in association with leukaemia and paraproteinaemas are discussed. Finally, the article considers the issue of 'overlap' syndromes--the occurrence of several paraneoplastic phenomena in the same patient.

Humans↗

[Role of electrophysiology in diagnosis of polyneuropathies].

Most for polyneuropathies present in a uniform, distally accentuated, rather symmetrical pattern, although asymmetric or multifocal distributions occur. The main feature of diagnosis is the history of development and the neurological clinical examination. Neurophysiologic studies, mainly nerve conduction studies (motor and sensory), reflex studies and electromyography are very accurate, but unspecific tools in order to establish the diagnosis of polyneuropathies, define special electrophysiologic features and can also reveal undetected (subclinical) lesions. For clinical purposes most neuropathies can be divided according the nerve conduction studies in axonal, demyelinating and mixed types. In recent years additional electrophysiological features as conduction block have appeared and are still under discussion. The etiology of polyneuropathy has to be determined in each patient with scrutinity. Additionally to general diseases (e.g. diabetes), common toxins (e.g. alcohol), concurrent medication (e.g. some cytostatic drugs) also immunologic (e.g. vasculitis) and hereditary factors have to be considered. A nerve biopsy is only indicated after a thorough consideration of electrophysiology and ancilliary findings. This applies in particular to hereditary neuropathies, where genetic testing has become a highly reliable test replacing biopsy.

Diagnosis, Differential↗

Light chain myeloma with oro-pharyngeal amyloidosis presenting as bulbar paralysis.

A 53-year old woman developed slowly progressive dysarthria, mild enlargement of the tongue and dysphagia since 1 year ago. All neurological differential diagnoses that could have explained the bulbar symptoms were excluded. The swallowing sequence was pathologic and immunoglobulins were markedly reduced. A bone marrow biopsy revealed light chain myeloma grade III. Amyloid deposits were found in the tongue but not in the kidneys. Oro-pharyngeal amyloidosis was held responsible for the described complaints. It is concluded that multiple myeloma must be considered in the differential diagnosis of bulbar paralysis and that biopsy of specific lesions is necessary to confirm local amyloidosis.

Amyloidosis↗

Antibodies of the anti-Yo and anti-Ri type in the absence of paraneoplastic neurological syndromes: a long-term survey of ovarian cancer patients.

In recent years several authors have described a close correlation between circulating antineuronal antibodies of different types and the occurrence of paraneoplastic neurological syndromes. Because this has not been widely accepted, we screened 300 serum samples from 181 ovarian cancer patients for the presence of circulating antineuronal antibodies by immunofluorescence. The findings were confirmed by immunoblotting. In 11 patients circulating antineuronal antibodies were detected. In 4 patients they were classified as anti-Yo and in 7 as anti-Ri, titres ranging from 1:400 to 1: 204,800. All the patients underwent thorough neurological and neurophysiological investigations, with special regard to paraneoplastic syndrome. None of them had symptoms pointing to a paraneoplastic neurological syndrome, although patients were followed up to 2 years after the first examination. Thus the frequency of circulating antineuronal antibodies in ovarian cancer patients is higher than the frequency of paraneoplastic syndromes, and antibody positivity does not necessarily lead to the appearance of a neurological paraneoplastic syndrome.

Autoantibodies↗

MRI in patients with general paresis.

Few cases of MRI in neurosyphilis have been reported. We examined the value of MRI in patients with general paresis; MRI was performed on four HIV-negative patients with parenchymatous neurosyphilis. It demonstrated frontal and temporal atrophy, subcortical gliosis and, in one patient, increased ferritin in the basal ganglia. The progression of the lesions on MRI correlated well with the neuropsychiatric disturbances. The MRI findings correlated with the well-known neuropathological findings. This combination of pathological findings in neurosyphilis has not been described before and we suggest that MRI is of prognostic value in patients with general paresis.

Adult↗

Vinorelbine-induced neurotoxicity in patients with advanced breast cancer pretreated with paclitaxel--a phase II study.

Vinorelbine (VNB) shows high antitumoral activity in advanced breast cancer due to its high affinity for mitotic tubulin and differs from the other vinca alkaloids with regard to its low degree of neurotoxicity because of its low affinity for axonal tubulin. Preclinical data show the existence of different binding sites on tubulin for vinca alkaloids and paclitaxel (P), suggesting a lack of cross-resistance. Thus, VNB was chosen eligible for a phase II study to evaluate both the therapeutic efficacy and the toxicity of VNB in patients (pts) with advanced breast cancer failing first- or second-line chemotherapy with P. A total of 14 pts with advanced breast cancer pretreated with P were entered into the study. Therapy consisted of VNB at 30 mg/m2 diluted in 500 ml of normal saline given over 30 min after a minimal interval of 4 weeks since the last application of P. For the first four cycles, injections were repeated at 2-week intervals; thereafter they were repeated at 3-week intervals until evidence of progressive disease or severe toxicity developed. All but one pt was considered assessable for response and all pts were evaluable for toxicity. No objective response was observed; two pts showed no change in their disease. In four pts therapy had to be stopped because peripheral neurotoxicity increased from a pretherapeutic level after therapy with P from National Cancer Institute Common Toxicity Criteria (NCI-CTC) grade 1 (n = 3) and 2 (n = 1) to neurotoxicity grade 3 after 1, 2 (n = 2), and 3 cycles of therapy with VNB, respectively. In addition, constipation of grade 2 occurred in 10 pts. Hematologic toxicity was negligible. No other evaluable toxicity exceeded NCI-CTC grade 1. Both observations of this study, the complete resistance to VNB and the increase in peripheral neuropathy, let us assume the existence of a preclinically not anticipated but clinically relevant cross-resistance between these two spindle poisons and the presence of common functional targets. Therefore, P-pretreated pts should be excluded from consecutive VNB-containing therapies.

Adult↗