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PubMed1991

[Stab wounds of the spinal cord by a kitchen knife: report of a case].

A case of spinal cord injury due to stab wounds by a kitchen knife is presented. A 41-year-old male was hospitalized because of spinal cord injury resulting from stab wounds inflicted with a kitchen knife in the posterior cervical area. Neurological examination on admission showed paraplegia, disappearance of deep tendon reflex in both lower extremities, sensory disturbance below T1 level, left Horner's syndrome and urinary disturbance. In addition to these symptoms cerebrospinal fluid was leaking from the wounds. An emergency operation was performed. After laminectomy of C7 and T1, we found that the spinal cord was almost completely split at C7/T1 level. Dural plasty was performed. Neurologically, sensory disturbance was slightly improved at 4 months after the injury. Initial MRI (TR: 200 msec, TE: 20 msec) revealed high intensity at C7/T1 level which was damaged by the kitchen knife. MRI 5 months after the injury revealed low intensity on T1 weighted imaged, high intensity on T2 and proton weighted image. The occurrence of the spinal cord injury due to stab wounds by a kitchen knife is very rare in Japan. MRI is useful in the diagnosis of stab wounds of the spinal cord.

Adult↗
PubMed1991

[An adult case of Chédiak-Higashi syndrome with parkinsonism and marked atrophy of the central nervous system].

Chédiak-Higashi syndrome (CHS) is often a fatal disease of childhood characterized by oculocutaneous forms of albinism with congenital gigantism of peroxidase granules, granulation anomaly of leukocytes, hereditary gigantism of cytoplasmic organelles and a marked susceptibility to infections. A few patients have survived to age 20 years. A 39-year-old woman developed tremor and gait disturbance at age 22 years. At age 25 years, she was admitted to the Hospital for evaluation. Mental impairment, horizontal nystagmus, bradyphrenia, cogwheel rigidity, tremor at tongue, mandible and hands, bradykinesia, and unsteady gait were found and a juvenile parkinsonism was diagnosed. However, there was no favorable response by levodopa therapy. She became unable to walk at age 33 years. On admission, Oct. 27, 1988, at age 39 years, she was bedridden with a posture of decorticate rigidity. She was found to have partial depigmentation of the retina and choroid, pale and atrophic optic disc and subluxation of the mandible, Onuaguluchi's finger deformities and pes cavus. Neurological examination disclosed that she was alert but had marked difficulty in speaking. The communication was only possible by giving a sign of grasping of the left hand. The patient also showed oculogyric crisis, dystonic rigidity of the neck, diffuse muscular atrophy, complete paraplegia and decreased deep tendon reflexes with Babinski sign. On laboratory studies, at age 39, the white cells count was decreased (2,510/mm3), the hemoglobin level was 10.3 g/dl, the serum iron was 12 micrograms/dl, IgG 2,828 mg/dl, IgA 1,002 mg/dl, and the activity of natural killer cell was profoundly decreased (2%, normal; 18-40). Hematological examination revealed peroxidase positive giant granules in leukocytes. Chest X-ray film disclosed marked abnormal colon gas which located right subdiaphragma (Chilaiditi syndrome). Cerebrospinal fluid contained 12 cells/mm3, 99% lymphocytes; protein, 58.8 mg/dl; IgG, 6.8 mg/dl; HVA, 4.5 ng/ml (normal 41.8-44.6); 5-HIAA, 1.3 ng/ml (11.3-29.2); MHPG, 5.8 ng/ml (13.2-22.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[A clinicopathological study of the somatic motor efferents in the pseudopolyneuritic form of amyotrophic lateral sclerosis].

Histopathology of the somatic motor efferents of three cases with pseudopolyneuritic from of amyotrophic lateral sclerosis (ALS) was analyzed, and the results were correlated with the clinical symptoms. The population of myelinated fibers in the lateral corticospinal tract at the thoracic segment, and in the fourth ventral roots, and motor neurons in the fourth ventral horns were morphometrically quantified. The patients were two males and one female ranging in age from 43 to 67 years, and showed a clinical course of 1.8 to 9.5 years. All three cases did not show any pyramidal sign nor spasticity but showed an extensive leg involvement, particularly the distally accentuated muscular weakness with depressed deep tendon reflexes. The clinical manifestations were consistent with the pseudopolyneuritic form of ALS. Fiber size profile of the myelinated fibers in the lateral corticospinal tracts at T7 segments and L4 lumbar ventral roots were estimated on the epon-embedded transverse sections as previously described (Sobue et al, 1981). Number and size distribution of anterior horn cells in the L4 segments were measured on 300-500 consecutive 10 microns-thick paraffin sections stained with Klüver-Barrera technique, using a TGZ-3 particle size analyzer (Zeiss). The location of the remained anterior horn cells was also quantitatively estimated. Three cases with common form of ALS and three control cases were analyzed in the same manner. The large myelinated fibers in the lateral corticospinal tract were extensively and predominantly depleted in all three cases. The small myelinated fibers were also depopulated but in lesser degree. The mode of these myelinated fiber loss was almost compatible with those in common form of ALS.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[A case of epidural lipomatosis presenting spinal ataxia].

A 41-year-old man was doing well until July 1989, when he noted numbness over soles, followed 4 months later by difficulty in walking. These symptoms were progressively getting worse, and he was admitted to our department on June 12, 1990. General physical examination was unremarkable. Neurologically cranial nerves were intact except old right, traumatic strabismus. Muscle tone and deep tendon reflexes were normal throughout, but bilateral Babinski and Chaddock reflexes were present. Mild weakness of lower extremities were found on muscle testing (4/5). In sensory system, superficial sensory disturbance below T10 was seen, and markedly diminished vibration and position senses of lower extremities were noted. Cerebellar test was intact, although unsteadiness was found on heel-shin test. Romberg sign was definitely positive. His gait was wide-based and ataxic. Laboratory data showed no abnormalities in CBC, chemistry, urinalysis, serological tests and endocrinological examinations. Spinal MRI (Siemens 1.5 Tesla) showed abnormal deposition of epidural fatty tissues compressing spinal cord with flattening of cord from T4 to T8. Spinal ataxia as compressive myelopathy due to epidural lipomatosis was considered and he underwent laminectomy from T4 to T8 with improvement in walking. Epidural lipomatosis is an unusual cause of spinal cord compression, presenting compressive myelopathy, radiculopathy, cauda equina syndrome, intermittent claudication, or back pain. Most of cases were associated with long-term administration of adrenocortical steroid hormone, or underlying diseases, except only 3 cases including ours. This is the first case of spinal epidural lipomatosis presenting progressive gait disturbance due to spinal ataxia.

Adult↗
PubMed1991

[A case report of the compression syndrome due to hypertrophic neuropathy].

We reported a case of hypertrophic neuropathy of adult onset. The pathological change in the sural nerve was decreased axonal population with onion-bulb formation. On examination, there were enlarged nerve on palpation and she was found to have distal muscle atrophy, weakness and sensory loss. The deep tendon reflexes of extremities were weak. The first clinical feature of this patient was mainly polyneuropathy. The lower limbs were slightly spastic and plantar responses were extensor bilaterally. There was also sensory level at C6 level. After 1.5 years from first examination, she had shown myelopathy. Magnetic resonance imaging (MRI) of the spine showed marked thickening of the nerve roots and it revealed the compression of the spinal cord by enlarged nerve roots from C2 to C6 level. The compression syndrome of the patients with hypertrophic neuropathy was unclear at the onset in this case. MRI study of the spinal cord would be very beneficial to disclose subclinical myelopathy associated with hypertrophic neuropathy, as indicated in this report.

Female↗
PubMed1990

[An autopsy case of complicated form of spastic paraplegia with amyotrophy, mental deficiency, sensory impairment, and parkinsonism].

An autopsied case of complicated form of spastic paraplegia with many unusual clinical and pathological features is reported. Present case: a 31-year-old male. His parents are first cousins. Pregnancy and delivery had been unremarkable. Though he was mentally retarded, his physical development was normal. He was considered normal until age 10. He suffered from progressive disturbance in gait at the age of 11. He could not walk without assistance at the age of 22. Neurological examination revealed the following findings. He was obese and mentally deteriorated. Spastic paraplegia with increased tendon reflexes and pathological reflexes was prominent. Though slight sensory disturbance was present in the lower extremities, neither involuntary movement nor cerebellar ataxia was observed. In the age of late 20's, dementia, general muscular atrophy, and Parkinsonism developed. At the age of 30, he could not move by himself. He was apathic and indifferent, and showed forced laughing. Muscle tonus was flaccid because of general muscular atrophy and peripheral neuropathy. He died of acute gastric enlargement. Neuropathological findings were characterized by mal-development of the central nervous system (CNS) and the multisystem degeneration. There existed cerebral white matter hypoplasia with hypogenesis of the corpus callosum and ectopia of neurons of the cerebral and cerebellar cortex. Hypoplasia of melanin pigment was also observed in the remaining neurons of the substantia nigra and the locus ceruleus. Many neurons in the CNS included lipofuscin granules of variable shapes. Some of them showed clusters of several block-like inclusions which were green with luxol fast blue and cresyl violet stain.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Motor neuron disease with Parkinson's disease--case report].

The patient was a 64-year-old woman who showed muscle weakness and tremor of upper extremities and gait disturbance at the age of 62 years. The symptoms progressed and she was admitted to our hospital. Neurological examination revealed muscle weakness, muscle atrophy and fasciculation bilaterally in the upper extremities. The deep tendon reflexes were reduced in the upper extremities and increased in the lower extremities, but Babinski's sign was not present. There was mild hand tremor at rest (right greater than left). Muscle rigidity was also evident. Her gait was small-stepped and her trunk was bent forward. She showed hypomimia, but no dementia was detected. She died of respiratory failure 7 months after admission. The duration of the illness was about 2 years. At autopsy, macroscopic examination showed depigmentation of the substantia nigra and locus ceruleus, and atrophy of the anterior roots of the spinal cord. Microscopic examination revealed a few senile plaques in the temporal cortex. In the substantia nigra, the number of melanin-containing cells was decreased in its central parts. A few Lewy bodies were found in some of the remaining neurons, and melanin pigment migrated into the parenchyma. In the locus ceruleus and dorsal motor nucleus of vagus, abundant Lewy bodies and mild astrocytosis were seen. A few Lewy bodies were also seen in the nucleus raphe, nucleus basalis of Meynert and hypothalamic nuclei. Severe neuronal loss of the anterior horn cells was observed in the cervical segment, and to a lesser degree, in the lumbo-sacral segments. segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain↗
PubMed1978

A familial neuronal disease presenting as intestinal pseudoobstruction.

The purpose of this paper is to describe 2 siblings who had a generalized neurological disease which presented as intestinal pseudoobstruction. The siblings had 40-year histories of abdominal pain, distention, and vomiting as well as gait ataxia, small, irregular, poorly reactive pupils, dysarthria, absent deep tendon reflexes, and impaired vibratory and position senses. Compared with age-matched controls, they had inappropriate blood pressure responses to phenylephrine, the Valsalva maneuver, and upright posture, lack of sweating on warming, and pupillary denervation hypersensitivity. Radiographs revealed hyperactive, nonpropulsive contractions of a dilated esophagus and small intestine and extensive colonic diverticulosis. Esophageal manometry recorded repetitive, spontaneous, nonperistaltic waves and positive Mechyolyl tests. Postmortem examinations showed degeneration of the myenteric plexuses of the esophagus, small intestine, and colon of both patients. Myenteric plexus neurons were significantly reduced in number compared with 7 controls. About one-third of the siblings' neurons contained round, eosinophilic intranuclear inclusions, which, by histochemistry, were composed of protein by lacked RNA, DNA, carbohydrate, and fat. By electron microscopy the inclusions consisted of an irregular array of nonviral, nonmembrane-bounded filaments. Neurons and glial cells of the brain, spinal cord, dorsal root, and celiac plexus ganglia contained identical intranuclear inclusions. Intestinal smooth muscle was normal. These 2 siblings represent a unique disease in which degeneration of the myenteric plexus resulted in hyperactive but uncoordinated smooth muscle activity and the clinical syndrome of intestinal pseudoobstruction, the presenting manifestation of their neurological disease.

Brain↗
PubMed1990

[An autopsied case of manifesting chorea, serum antibody to brain proteins, neuronal degeneration in striatum and grumose degeneration in dentate nucleus].

A 49-year-old man complained of difficulty in writing due to choreic involuntary movement in the right hand, which spread gradually to his left hand, face, lower extremities and trunk during next nine years. He also showed difficulties in speech and swallowing. His family noticed his memory disturbance and change of his character. Ten years later, mental deterioration, dysarthria and dysphagia were manifested. He showed facial grimacing and dancing gait. Deep tendon reflexes were exaggerated with no pathological reflexes. Muscle tone was rigid at his ankles. He showed no ataxia nor sensory impairment. At about 61 years old, choreic movement was decreased and rigidity spread in all extremities with joints' constructure. During next one or two years, choreic movement diminished and was restricted to his face. The extremities became more rigid and voluntary movement was severely impaired. He became mutistic with severe mental deterioration. He died at the age of 65. None of his family suffered from the same disease. Routine blood examination was normal, and there were no acanthocytes. Brain CT showed marked dilatation of lateral and third ventricles, and mild cerebral cortical atrophy. The head of caudate nucleus was also atrophic. The total protein level in the CSF was elevated to 79-121 mg/dl, and IgG% was 13.7-26.6 for last six years. Anti-CNS antibodies in the serum reacted with brain proteins of 156 kDa and 82 kDa. Pathological examination showed severe atrophy of the caudate nucleus, putamen, globus pallidus, cerebral cortex and cerebral white matter.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Polyneuropathy: potential cause of difficult weaning.

Severe critically ill polyneuropathy (CIP) is a neurologic syndrome with potential effects on ventilatory weaning. Fifteen CIP patients with the following clinical criteria were diagnosed: limb weakness, amyotrophy, and reduced deep tendon reflexes. Electromyogram (EMG) confirmed polyneuropathy by the following signs: denervation, normal nerve conduction velocities, normal distal latencies, and decreased compound action potential. It was observed that motor signs were more important than sensitivity. EMG performed during ICU hospitalization showed axonal abnormalities. Ventilation and mean duration of weaning were unusually long. Four patients had EMG a few years after discharge; the recovery was delayed and incomplete. The present study suggests that CIP is a multifactorial disease.

Action Potentials↗
PubMed1990

[A case of delayed radiation lumbo-sacral plexopathy].

We report a 47-year-old woman who developed a slowly progressive lumbosacral plexopathy with mixed sensorimotor losses in the lower extremities. The symptoms were apparent 8 years after x-ray irradiation for an ovarian carcinoma. Neurological examination showed mild weakness and absent deep tendon reflexes of bilateral lower extremities, and hypesthesia to all modalities in anterior aspects of bilateral lower thighs, in dorsum pedis and soles. Extensive investigations regarding the possibility of tumor recurrence were negative. Computed tomography of pelvis showed abnormal soft tissue densities around the lumbosacral plexus. Intravenous pyelography showed bilateral hydronephrosis and narrowed ureters at the first sacral vertebra level. These findings are consistent with radiation-induced fibrosis rather than tumor infiltration. The results suggest the entrapment lumbosacral plexopathy due to surrounding fibrosis after irradiation. We speculated the sensorimotor losses caused by entrapment of the lumbosacral plexus.

Female↗
PubMed1990

[Eaton-Lambert syndrome manifested by respiratory failure associated with small cell carcinoma of the lung].

A 63-year-old man with Eaton-Lambert syndrome manifested by marked respiratory failure was reported. He began to notice blepharoptosis and diplopia in September, 1987, followed by weakness and easy fatigability in bulbar, neck and limb muscles in association with impotence by February, 1988. On admission in August, 1988, Gowers' sign, decreased tendon reflexes and muscle weakness improved by the injection of edrophonium were found. Anti-acetylcholine receptor antibody was negative. Single muscle action potential evoked in the thenar muscle was abnormally low in amplitude with the stimulation of the median nerve: repetitive nerve stimulation study revealed the waning at the low rates, but the waxing at the high rate (30 Hz), suggesting the diagnosis of Eaton-Lambert syndrome. Early gastric cancer (adenocarcinoma) was diagnosed from needle biopsy specimens in August, 1988, but no other neoplasm including thymoma or lung cancer was found. After subtotal gastric resection in September, 1988, he failed into respiratory failure, requiring artificial ventilation for seven months. Plasmapheresis and drugs such as anticholinesterase, guanidine hydrochloride, and corticosteroid were ineffective for the recovery from weakness in respiratory muscle. Lung cancer was suspected, based on a chest X-ray in March, 1989, and one month later he died of pneumonia. At autopsy, small cell carcinoma of the lung was observed, but there was neither recurrence nor metastasis of the gastric cancer. Emphasis was placed on the respiratory failure in Eaton-Lambert syndrome which has rarely been reported.

Adenocarcinoma↗
PubMed1990

[Neurophysiological studies on group A xeroderma pigmentosum in early childhood].

Neurophysiological studies were performed on 8 patients with group A xeroderma pigmentosum during early childhood. EEG, ABR and NCV were normal during this period. In contrast, various sleep parameters detected by polysomnography showed abnormal findings even in the neurologically normal patient. Decreased % sleep REM was seen in a case, and decreased frequency of REMs were seen in another. Body movements were extremely high or low in frequency in 3 cases in whole night sleep. The distribution of body movements were abnormal; in control subjects, the frequency was higher in SREM and stage 1 than in slow wave sleep; in 7 cases, it was higher in slow wave sleep than in stage 1 or 2, or body movements were extremely frequent. Neurological examination revealed soft signs in various systems in early childhood. All cases except one showed hypotonia. Many cases were slow in learning to walk and the gait was unstable. Speech delay and decreased deep tendon reflexes, especially of patella, were seen in most cases. Since the neural deficits in XP may be related to the DNA repair defect, these findings indicate the possibility that some endogenous compounds distributing all over the nervous system might produce the DNA damages. Because the body movements during sleep are controlled by the nigrostriatal dopaminergic system, present data indicate that the basal ganglia might be one of the earliest degenerative systems in the CNS. Recently, some studies have suggested the possibility that oxygen radical mechanisms might be involved in the development of the dopamine neurodegenerative process in Parkinson's disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1990

[Remarkable effect of class Ib Na channel blocker on painful alcoholic neuropathy].

Two cases of painful alcoholic neuropathy are reported. The pain in both cases were incurable by using pain killing drugs, but administration of class Ib Na channel blocker, mexiletine, was remarkably effective. In the first case, suspension of drug administration produced the recurrence in the pain. Objective findings, for example, deep tendon reflex, vibration sense, and nerve conduction velocity, did not change significantly, after medication. And the only side effect was hot sensation in the lower extremities. We report the pain killing effect of class Ib Na channel blocker on painful alcoholic neuropathy, that has not yet reported.

Alcoholism↗
PubMed1990

[A manifesting carrier of Duchenne muscular dystrophy presenting mosaic distribution of dystrophin negative and positive muscle fibers].

A 25-year-old female patient with an approximate 10-year-history of slowly progressive muscle weakness was diagnosed as a manifesting carrier of Duchenne muscular dystrophy (DMD) because her muscle biopsy showed scattered fibers with no dystrophin on immunohistochemical staining. She had no family history of neuromuscular disorders. She was in good health until about 14 years of age, when she developed muscle weakness and atrophy of the extremities with slow aggravation. On admission at the age of 25 years, she had asymmetrical muscle atrophy in the lower extremities; the left femur, right femur, left crus, and right crus measured 36.0, 40.5, 31.5, and 35.5 cm in circumference, respectively. However, the muscle weakness of the extremities was symmetrical with no laterality, and the proximal muscles in the lower extremities were predominantly affected to 3+/5 MMT test. She walked with a mild wadding manner and stood up with Gower' maneuver. Deep tendon reflexes of the extremities were almost normoactive with no pathologic reflexes. As to laboratory findings, serum enzymes of muscular origin were elevated; GOT was 44 IU/l, GPT 60 IU/l, LDH 829 IU/l, CK 4238 IU/l, and aldolase 31 SL units. The electromyogram showed myopathic changes mixed with some neurogenic components. Peripheral nerve conduction velocity was normal. A computed tomography of the skeletal muscles showed more marked atrophy and lower density in the left lower extremity than in the right. The biopsied left gastrocnemius muscle demonstrated a marked variation in fiber size with some necrotic and regenerating fibers. On immunohistochemical stain with anti-dystrophin antibody, the dystrophin negative fibers were scattered among positive fibers in a mosaic distribution.

Adult↗
PubMed1990

[An autopsy case of amyotrophic lateral sclerosis associated with cervical syringomyelia].

An autopsied case of amyotrophic lateral sclerosis complicated by cervical syringomyelia was reported. The case was a 59-year-old man, who first noticed weakness of both lower extremities at 54-year-old. The weakness spread to both upper extremities within 2 years. Cervical myelography revealed multi-level cervical spondylosis and anterior fusion of C5-C7 was done. But the weakness and atrophy of proximal muscle, diminished deep tendon reflex on upper extremities, hyperreflexia and pathological reflexes on both legs, tongue fasciculation and respiratory muscle weakness developed successively, and the patient died of respiratory distress at 59-year-old. Autopsy revealed multiple independent four syrinxes located at the level between C2-C7. One of these syrinxes had ependymal cell lining and thought to be idiopathic syringomyelia. The other three syrinxes were considered to be the cavitation in association with cervical spondylotic myelopathy. Degeneration and decreasing of spinal anterior horn cells, atrophy of medullary pyramis and Bunina bodies were observed as features of typical amyotrophic lateral sclerosis. Cervical spondylosis as causative lesion of multiple syrinxes was discussed, and relationship between ALS and the syrinxes was not indicated clearly.

Amyotrophic Lateral Sclerosis↗
PubMed1990

[A new family of Machado-Joseph disease--an abnormal decrease in signal intensity of the putamen in magnetic resonance imaging].

The propositus (case 1) was a 40 year-old man. He had begun to note unsteady walking at age 26. He was found to have cerebellar ataxia and pyramidal signs in addition to minor features such as progressive external ophthalmoplegia, gaze nystagmus, bulging eyes, intention fasciculation-like movements of facial and lingual muscles, and limb dystonia. These findings were categorized into type II form of the disease. One sister (case 3) aged 37 years, and one brother (case 4) aged 44 years of the propositus had also type II form of the disease. His uncle (case 2) had the same cerebellar and extrapyramidal signs accompanied with peripheral nerve signs such as muscle wasting, weakness, hypo-tonus and decreased deep tendon reflexes, and a diagnosis of type III form of the disease was made. In the T2-weighted magnetic resonance imaging (1.5 T, TR 2000 or 3000 msec, TE 120 msec) of the three patients (case 1, 3 and 4), dorsolateral part of the putamen showed decreased signal intensity. Although hypo-intensity of the putamen is often observed in normal elderly people over 50 years old, it is considered to be abnormal when it exists in relatively young people as in this family members.

Adult↗
PubMed1990

[Intradural extramedullary tumor of lower spinal cord in a 89-year-old man with cervical spondylosis and lumbar spondylolisthesis].

A 89-year-old man was admitted because of slowly progressive gait disturbance during these several years. Neurological examination revealed paraparesis with bilateral sensory disturbance in the lower extremities, more severely on the left side. Vibration sense was almost completely disturbed under the level of bilateral crista iliaca. Deep tendon reflexes decreased in the lower extremities. No urinary incontinence was observed. The narrow spinal canal and cervical spondylosis were seen at the C 5-6 level, showing the anterior-posterior distance of 10 mm. Computed tomography of the lumbar spine showed spondylolisthesis between the level 4 and 5. CSF showed high protein concentration (300 mg/dl), whereas normal cell counts. These findings suggested the following two possibilities; cervical myelopathy associated with the disturbance of the cauda equina due to lumbar spondylolisthesis, or the disturbance at the lower thoracic or upper lumbar level of spinal cord. The spinal MRI revealed the irregular mass lesion in the lower spinal cord at the level of spine Th 11-12 on T2 weighted images, with enhancement by Gd-DTPA on T1 weighted images. These MRI findings suggested the intradural extramedullary tumor, such as benign neurinoma or meningioma. No clear cut lesions were found at the cervical spinal cord or at the cauda equina. MRI was useful for the diagnosis of sites and lesions of spinal cord in the present case, whose neurological signs and symptoms could be explained by the coexistent cervical spondylosis and lumbar spondylolisthesis.

Aged↗