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The urological manifestations of the tethered spinal cord.

The tethered cord is the fixation of the cord resulting in stretching as growth occurs. In this paper, three cases of tethered cord with symptoms related to the urinary tract were presented. In the first case, a 12-year-old girl presenting with abdominal pain and urinary incontinence had bilateral hydronephrosis and neurogenic bladder due to a tethered cord without having any other neuropathological manifestation. In the second case, an eight-year-old girl presented with enuresis and a mass in her back was found to have a lipomyomeningocele, hyperactive tendon reflexes in the lower limbs and pes cavus. Tethered cord associated with lipomyomeningocele caused a neurogenic bladder and bilateral hydronephrosis. In the third case, a seven-month-old girl presented with hydrocephalus as well as bilateral dilation of the renal pelvis, unilateral ureteral duplication and vesicoureteral reflux. A tethered cord was revealed in this patient, who had a meningomyelocele operation in the neonatal period. Renal function test in the first two cases were abnormal.

Child↗
PubMed1994

[Bone pain, polydipsia, polyuria].

This 20 year old man suffered increasingly from multifocal bone- and back pain over the last 6 months. Painful weakness of the left leg with dysesthesia of the 4th and 5th toe, a weight loss of 15 kg and polydipsia and pollakiuria had developed. The clinical workup disclosed hard tumors in the right mandible and tibia, a waddling gait with bilateral sign of Trendelenburg, reduced muscular force in the left leg with missing achilles tendon reflex and a loss of sensibility in the distal S1 segment, epigastric tenderness on pressure and hypertension with a value of 160/100 mmHg. X-rays revealed multiple cystic bone lesions at all sites. Hypercalcemia and massively elevated parathyroid hormone were measured. Since the parathyroids were enlarged on sonography, primary hyperthyroidism with fibrosing osteitis v. Recklinghausen was diagnosed.

Adenoma↗
PubMed1994

Examination of the segmental pathophysiological mechanisms of spasticity.

The purpose of this investigation was to ascertain a complex of electromyographic methods suitable for evaluation of the basic segmental pathophysiological mechanisms of spasticity. Clinical and electromyographic examinations were performed on 120 patients with spastic hemiparesis after stroke. Patients muscle tone, muscle force and tendon reflexes were assessed by the well known clinical five point scales. A battery of electromyographic methods was used to analyze different segmental mechanisms of spasticity: for alpha motoneurone activity--the F-wave parameters; for gamma motoneurone activity--the TA/H amplitude ratio; for common interneurone activity--the flexor reflex parameters; for presynaptic inhibition--the Hvibrated/Hmaximal amplitude ratio. Our results revealed that nearly all of the patients have increased alpha motoneurone activity on the spastic side. In most of the patients at least two of the segmental mechanisms are altered. Different mechanisms participate with different frequency in development of spasticity. We suppose that alpha-motoneurone hyperactivity usually develops secondary after alteration of some other segmental mechanism. In conclusion the applied complex of electromyographic methods gives the possibility for evaluation of the individual pathophysiological profile of patients with spasticity. This is a background for appropriate treatment.

Aged↗
PubMed1993

[Polyneuropathies--symptoms, causes and diagnostic procedure].

The diagnosis of a polyneuropathy (PNP) is particularly a clinically based diagnosis. The polyneuropathic syndrome consists of typical symptoms like paraesthesias, pain, cramps and fasciculations as well as characteristic signs like loss of tendon reflexes, weakness and wasting of muscles, sensory loss, cranial nerve palsy and alterations of the autonomic nervous system. The analysis of manifestation-types is very important for the differential diagnosis. The symmetrical sensory type of manifestation can be found in the beginning of almost all toxic neuropathies as well as in uremic and diabetic neuropathy. The symmetrical-motor type of manifestation can be a further development of the symmetrical sensory type of manifestation or exists from the beginning in the case for example of Guillain-Barré-Syndrome. The asymmetric type of manifestation can be observed in the vascular neuropathies and in some types of inflammatory neuropathies like the neuroborrelioses or the neuralgic amyotrophy. The investigation of the CSF, electromyography and electroneurography as well as a great number of chemical lab tests are important for the etiological classification. According to the etiology, the polyneuropathies can be subdivided into four groups such as inflammatory, vascular, exotoxic and endotoxic-metabolic-hereditary diseases. The most frequent etiologies are diabetes mellitus and chronic alcoholism.

Diagnosis, Differential↗
PubMed1994

[Myopathy, cerebellar ataxia and Williams syndrome like features in siblings].

Two female cases, 23- and 21-year-old, of supravalvular aortic stenosis associated with cerebellar hypoplasia, retinitis pigmentosa and myopathy were reported. No family history of mental retardation and cardiovascular anomalies was found. There was no consanguinity between the parents. Pregnancy, labor and delivery were reported to be uncomplicated. When they visited to our hospital at the age of 13 and 11 years, they had short stature, characteristic facial appearance (eg, wide mouth, elongated philtrum, low nasal bridge and broad forehead) and supravalvular aortic stenosis. Neurological examination disclosed mental retardation, retinitis pigmentosa, muscle wasting and contracture of bilateral knee and ankle joints. Gait was unsteady and bradykinetic. Their smooth pursuiting ocular movements were saccadic. No nystagmus was recorded. Mild intention tremor was present. The muscles were slightly hypotonic, but deep tendon reflexes were hyperactive in the lower extremities. The sensory system was normal. Results of chromosome analysis and urine amino acid analysis were normal. The serum creatine kinase was elevated to 1,000-3,000 U. Muscle biopsy revealed nonspecific myopathic changes such as variability of fiber diameter in both fiber types. Neither cell infiltration nor deposits of fat or glycogen was found. Cranial MRIs performed at the age of 22 and 20 years disclosed cerebellar hypoplasia and moderate enlargement of the fourth ventricle. The two cases resembled clinically those of Williams syndrome, but the MRI findings were not consistent with those of the syndrome. The disorder is considered to be either Williams syndrome complicated by some other relatively rare clinical features, or another heredofamilial disease partly resembling Williams syndrome.

Adult↗
PubMed1994

[A case of cervical spondylitis mimicking motor neuron disease].

The patient was a 65-year-old man who had noted mild weakness of the right hand since summer, 1990. In October, 1990, he had fever and developed apparent weakness of the upper extremities. Neurological examination on admission revealed distal dominant muscle weakness and atrophy of the upper extremities with fasciculation. Deep tendon reflexes were diminished in the upper limbs and exaggerated in the lower ones. No sensory disturbance or cerebellar signs were recognized. Laboratory examination of his blood showed leukocytosis and elevated levels of acute reactants. The needle EMG showed a neurogenic pattern. MRI study of the neck disclosed narrowing of the intervertebral space between C7 and Th1 and a low signal intensity of these vertebral bodies on T1 weighted image. Treatment with antibiotics improved his neurological symptoms and the abnormal MRI findings. The present case was diagnosed as having cervical spondylitis. Neurological symptoms and signs associated with cervical spondylitis have been reported to be paraplegia or quadriplegia. Like the present case, however, cervical spondylitis should also be considered as one of the diseases which could show symptoms and signs very similar to those of motor neuron disease.

Aged↗
PubMed1993

[Ossification and calcification of the cervical ligamentum flavum--case reports].

Ossification of ligamentum flavum was reported usually lower thoracic and lumbar region, and rarely seen in the cervical region. Calcification of cervical ligamentum flavum is also relatively rare. We report a case of ossification and another of calcification of cervical ligamentum flavum, and discussed the difference of the clinical and radiological features in these conditions. Case 1: A 55-year-old man presented with numbness of the left shoulder and urinary dysfunction. Neurological examination revealed weakness, muscle atrophy and elevated deep tendon reflexes of the left extremities. CT showed ossified mass protruding into the right side of the canal and compressing the spinal cord at C 3/4 and C 4/5. MRI showed low intensity mass both on T1- and T2-weighted images and severe compression of the spinal cord. Left side partial hemilaminectomy with foraminotomy, so called "key hole" foraminotomy, satisfactorily decompressed the cord with clinical improvement. Case 2: A 70-year-old woman complained numbness of both hands for two years. She had sensory disturbance of both hands and spastic gait disturbance. Cervical X-ray films showed calcified nodules on the inner surface of lamina at C4/5. Axial CT demonstrated calcification in the ligamentum flavum at the C4/5 and C5/6 levels. MRI showed posterior spinal cord compression at the C4/5 and C5/6 levels. Osteoplastic laminotomy and removal of the affected ligamentum flavum were performed with successful result. Only 8 cases ossification of cervical ligamentum flavum above C6/7 have been so far reported. All are Japanese; four male and four female cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[A case of flaccid paraplegia associated with HTLV-I infection].

A 63-year-old female began to have progressive gait disturbance at the age of 50. Neurologic examination revealed weakness and hypotonus of bilateral leg muscles. Deep tendon reflexes were hypoactive with positive Babinski sign and vibration sense was diminished in the legs. HTLV-I antibody titers were elevated both in serum (x 131,072) and in CSF (x 512). The result of nerve conduction velocities and short latency somatosensory evoked potentials suggested mild peripheral nerve lesion. Needle EMG studies showed myogenic changes in the upper limbs and also, neurogenic changes in the lower limbs. Histological examination verified mild myogenic changes in biopsied deltoid muscle and neurogenic and myogenic changes in the quadriceps femoris muscle, with ragged-red fibers. We consider that this patient has myelopathy, myopathy, peripheral neuropathy and anterior horn cell involvement associated HTLV-I infection. The relationship between HTLV-I infection and mitochondrial abnormalities of the biopsied muscles remains unclear.

Female↗
PubMed1993

[Acute progressive polyneuropathy in a patient with Waldenström macroglobulinemia].

A case of Waldenström's macroglobulinemia (WM) (IgM-kappa type) associated with acute-onset demyelinating peripheral neuropathy is reported. A 49-year-old woman was admitted to our hospital because of general fatigue and recurrent syncope attacks. She was treated with vincristine, cyclophosphamide, epirubicin and prednisolone. By 10th hospital day, her clinical condition improved and serum viscosity was reduced. However, on the 21st hospital day, she suffered from rapidly progressive writing and gait disturbance. Neurological examination showed muscular atrophy and weakness in the distal part of four extremities. Deep tendon reflexes were diminished. There was no sensory deficit. Cerebrospinal fluid was normal. Anti-myelin associated glycoprotein activity of her serum was negative. Both motor and sensory nerve conduction velocities were markedly decreased. Biopsy of sural nerve revealed marked demyelination and onion bulb formation. There was IgM deposition on myelin sheath. Minimal axonal changes excluded the possibility of vincristine neuropathy. Plasmapheresis improved her symptoms, but nerve conduction velocities remained unchanged. Polyneuropathy associated with WM is usually gradual onset and sensory dominant. In this case, associated neuropathy was acute onset, progressive and motor dominant. This type of neuropathy in patients with WM is very rare.

Acute Disease↗
PubMed1993

[Distal myopathy with rimmed vacuoles and sudden death--report of two siblings].

We describe two siblings with distal myopathy with rimmed vacuoles, who died suddenly presumably due to fatal arrhythmia. Case 1. A 26-year-old man with a 4 year-history of progressive muscle weakness and wasting was hospitalized in April, 1989. The family history showed that his younger brother had the same disease, but his parents, not consanguineous, and other family members had no neuromuscular diseases. On admission, neurologic examination showed muscle weakness and atrophy in the distal portions of four extremities. No myotonia or fasciculation was present. The deep tendon reflexes were absent except diminished bilateral PTR. Sensation and co-ordination were normal. The creatinine kinase (CK) level was moderately elevated to 691 IU/l, and the aldolase mildly to 6.9 IU/l. Normal laboratory values included serum electrolytes, glucose and thyroid function study. An ischemic forearm exercise test revealed a normal rise in serum lactate and pyruvate concentrations. The glucose response after glucagon was normal in the fasting state. An electrocardiogram and chest film were normal. An electromyogram revealed myopathic changes with mild neuropathic changes, including positive sharp waves and fibrillation potentials at rest. The muscle biopsy specimen from the left anterior tibial muscle showed scattered fibers with rimmed vacuoles and moderate variation in fiber size. Neither fiber necrosis nor inflammatory cellular infiltration was seen. Regenerating fiber was not present. An electron microscopic examination showed numerous lamellar bodies of various size. Nerve biopsy was normal. He was diagnosed as having distal myopathy with rimmed vacuoles. Muscle weakness progressed gradually over the next two years, but his general condition was good. He asked to receive the corticosteroid therapy, and rehospitalized.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Proximal lower motor neuron syndrome associated with serum antibodies to asialo-GM1, GM1 and LM1].

A 31-year-old man had noticed slowly progressive weakness in his right upper limb girdle. On admission at age 32, fasciculation and muscle atrophy were observed in the right pectoralis major muscle. There was mild muscle weakness in the right triceps brachii muscle. The deep tendon reflexes were normal and the pathologic reflexes were absent. Sensory and autonomic nerve functions were intact. Needle EMG showed fibrillation potentials and positive sharp waves in the right pectoralis major, infraspinatus, extensor carpi radialis, extensor digitorum muscles, the bilateral sternocleidomastoideus and triceps brachii muscles. Motor nerve conduction studies revealed normal conduction velocities and distal latencies as well as no evidence of conduction block or abnormal temporal dispersion. Serum immunoelectrophoresis failed to detect an M protein. Thin-layer chromatography with immunostaining revealed that the serum contained auto antibodies which reacted with asialo-GM1, GM1 and LM1. This case must belong to "proximal lower motor neuron syndrome" proposed by Pestronk et al.

Adult↗
PubMed1993

[A case of juvenile onset ataxia with dystonia, myoclonus, sensorineural hearing loss and mental retardation].

A 35-year-old female was reported who presented early onset and slowly progressive ataxia and retrocollis which appeared at the age of nine. On admission, neurological examination revealed cerebellar ataxia, dystonia of the neck and the right arm, myoclonus of the neck and the shoulder, slight mental retardation, supranuclear upper gaze palsy, and sensorineural hearing loss. Laboratory examination showed high serum CK activity. Electromyography and muscle biopsy findings suggested slight muscular involvement. CSF level of HVA and 5-HIAA were reduced. MRI demonstrated marked cerebellar atrophy and slight atrophy of the brain stem. To our knowledge, the characteristic combination of the neurological sign in this case has not been reported. This case was compared with EOCA (early onset cerebellar ataxia with retained tendon reflexes) and other juvenile onset cerebellar ataxia and dystonia.

Adult↗
PubMed1993

[Hereditary dentatorubro-pallidoluysian atrophy (DRPLA): clinical studies on 45 cases].

The term of dentatorubral and Pallidoluysian atrophy (DRPLA) was first introduced by Smith, who proposed that there was a combination of cerebellar ataxia with choreoathetosis based on DRPL lesions. In 1972, Naito et al. reported two families with progressive myoclonus epilepsy (PME) syndrome with cerebellar ataxia, and hyperactive deep tendon reflexes. In 1977, Oyanagi et al. reported 4 autopsied cases of PME, and pointed out degenerative lesions in the DRPL systems. In 1982, Naito and Oyanagi reported this type of PME to be hereditary DRPLA, with a clinicopathological disease entity. This type of PME with DRPLA has been made a major category, especially in Japan. In this article, clinicopathological features of the hereditary DRPLA will be reviewed on the basis of 45 patients with this disease. The disease was inherited as an autosomal dominant fashion, and induces a wide rage of clinical features depending upon the age of onset, ranging from 3 years to 69 years of age. The initial symptoms were variable according to the age of onset and mental retardation was the most prominent symptom in the patients in which the disease started in the first decade and with an epileptic seizure in the second decade. In the following next two decades, the incidence of epileptic seizure, as initial symptoms was decreased to 23% and gait disturbance and ataxia in 38% of the patients, which increased to 73% in the 5th and 6th decades. The cardinal symptoms of hereditary DRPLA includes mental retardation, epileptic seizure and myoclonus, cerebellar ataxia with gait disturbances, psychological symptoms including clonus, cerebellar ataxia with gait disturbances, psychological symptoms including character changes, and dementia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

[Unexpected movements in a brain-dead patient].

In a brain-dead patient, a 42-year-old woman who went into a coma after a cervical foraminotomy, spinal automatisms were seen which cast doubt on the diagnosis of brain death. The procedure which was to lead to organ transplantation was seriously disturbed. In brain-dead patients spinal automatisms appear earlier and are more often present than deep tendon reflexes. Due to the developing hyperreflexia spinal automatisms can be elicited more easily and from a larger skin area as the period of brain death lasts longer. Spinal automatisms can also appear spontaneously and can be generated by hypercapnia. If criteria for brain death are met, these movements are no reason to reconsider the diagnosis of brain death.

Adult↗
PubMed1993

[MRI findings in patients with acute autonomic and sensory neuropathy].

Acute autonomic and sensory neuropathy (AASN), characterized by acute onset of extensive autonomic dysfunction and severe sensory deficits, was first described by Colan et al. (1978). We present two female patients with AASN in whom magnetic resonance imaging (MRI) confirmed such findings in the posterior column of the spinal cord. One patient was a 44-year-old woman who developed an upper respiratory tract infection followed in 2 weeks by numbness of the limbs and gait disturbance. There was orthostatic hypotension with syncope, paretic ileus, anhidrosis and urinary retention. There was a loss of sensation over the entire body, including the face, and deep tendon reflexes were generally absent. Neurophysiologic studies showed that sensory nerve action potentials and SSEPs were not evoked in the nerves examined. Sural nerve biopsy demonstrated severe axonal degeneration of the myelinated and unmyelinated fibers. Our second patient, a 27-year-old woman, exhibited similar clinical and laboratory features. The autonomic dysfunction in both patients improved gradually without drug treatment, but the sensory deficits--predominantly a loss of deep sensation--persisted for several years. In both patients, MRI revealed the T2*-weighted high intensity area in the fasciculus gracilis of the posterior column of the spinal cord. Such high intensity areas were present in all spinal segments. The severe and persistent sensory disturbance in these patients may have been caused by a lesion of the posterior column of the spinal cord following the involvement of the dorsal root ganglion cells, or ganglioneuronopathy, as demonstrated by MRI.

Acute Disease↗
PubMed1993

[A case of hereditary motor and sensory neuropathy (HMSN type 2) with bilateral recurrent nerve palsy].

An atypical case of hereditary motor and sensory neuropathy (HMSN) type 2 with cerebellar ataxia, hand tremor and bilateral recurrent nerve palsy was described. The patient was a 57-year-old man who complained of dyspnea, stridor , hoarseness during exercise and snored heavily during sleep since he was 20 years old. These symptoms and signs were slowly progressive. He had difficulty in breathing even at resting state when he was 54 years old and since then, he noticed muscle wasting of his hands and feet. Neurological examinations on admission revealed pes cavus, scoliosis, distal muscular atrophy in his four extremities, especially severe in bilateral lower limbs. Deep tendon reflexes were diffusely depressed. The fiberscopic examination demonstrated the limitation of bilateral vocal cord abduction and his tongue was slightly atrophic. Fine postural tremor was found in bilateral hands. Mild limb and truncal ataxias were also noted. Blood pCO2 level was elevated to 66% although FEV1.0% and vital capacity were within normal limits. Peripheral nerve conduction velocities were almost normal, though distal terminal latencies were slightly prolonged and amplitudes of evoked potentials were markedly decreased. The sural nerve biopsy studies revealed the chronic axonal or neuronal degeneration of both large and small myelinated fibers. From the clinical, electrophysiologic and histopathologic findings, the diagnosis of HMSN type 2 with bilateral recurrent nerve palsy and other atypical neurological findings was made. It is practically important to evaluate the presence or absence of vocal cord paralysis in the patients with HMSN from clinical viewpoints.

Biopsy↗
PubMed1993

[A case of radiation myelopathy with characteristic findings of thermoregulatory sweat distribution and magnetic resonance images].

A 73-year-old man had undergone resection of a lung carcinoma of the right upper lobe in 1987. Post-operative irradiation (40 Gy) was given to the right hilus. In November 1988, recurrence was detected in the trachea. Laser therapy was done in December 1988. From January 9 to February 13 in 1989, irradiation (50 Gy) was given to the mediastinum. From the beginning of 1991, the patient developed muscle weakness in the right lower extremity and pain temperature sensations were impaired below the Th12 level on the left side. On October 3, 1991, he was admitted to our hospital. Neurological examination revealed mild muscle weakness in the right lower extremity. Superficial sensations were impaired below the Th6 level bilaterally. Deep tendon reflexes were hyperactive in the lower extremities. A bilateral Babinski sign was positive. The T1 weighted MRI showed a low signal intensity in the spinal cord at the level of thoracic vertebra (TV)2-TV6. T2 weighted images revealed a high signal intensity area of the spinal cord from TV4-TV6. A gadolinium-DTPA injection revealed an enhancement on the left side of the spinal cord at the TV2-3 level, and right side of the spinal cord at the TV4-5 level on the sagittal and axial images. A thermal sweating test revealed hypohidrosis below the Th8 level on the right side, and the Th11 level on the left side. Sweating was delayed at the Th7-8 levels on the right side and Th10-11 levels on the left side. An irradiated field on the chest revealed hypohidrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[A case of deletion of the short arm of chromosome 18 associated with chronic polymyositis].

A case of deletion of the short arm of chromosome 18 (18p- syndrome) associated with chronic polymyositis is described. The patient was a 37-year-old woman, who had psychomotor retardation in her early childhood. She started to notice a difficulty in raising both arms at 14 years of age and furthermore, she developed a gait disturbance due to weakness of the proximal muscles of the lower extremities from 34 years of age. Her parents were first cousins. On physical examination, she showed many dysmorphic features, such as short stature, round face, hypertelorism, low nasal bridge, small chin, high arched palate, abnormal dentition, short and webbed neck, and broad chest. Neurological examination revealed a low intelligence (IQ 47), severe proximal muscle weakness with moderate proximal muscle atrophy in all extremities, a waddling gait, and decreased or absent deep tendon reflexes of all extremities except for bilateral ankle jerks. Serum creatine kinase and myoglobin levels were slightly elevated. Needle EMG study showed fibrillation potentials at rest and polyphasic and low amplitude motor unit potentials of short duration on volitional activity in the affected muscles. Muscle biopsy demonstrated a variation in fiber size, necrotic fibers and mononuclear cell infiltration. These findings were compatible with those of chronic polymyositis. In addition, cytogenetic findings revealed 46.XX.18p- karyotype, although her parents had no chromosome abnormality. She had no immunological abnormality except for a positive rheumatoid factor and elevation of CD4/CD8 ratio on lymphocyte subset analysis in peripheral blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗