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PubMed1995

[A case of spinal dural arteriovenous fistula associated with normal pressure hydrocephalus].

A 62-year-old male presented with urinary incontinence, gait disturbance and dementia for 6 months. Neurological examination revealed severe paraparesis (1/5), sensory disturbance below Th10, neurogenic bladder and absence of patellar and achilles tendon reflexes. CT scan showed mild brain atrophy and symmetric ventriculomegaly with periventricular lucency. Magnetic resonance imaging (MRI) showed a linear flow void lesion on the dorsal surface on the back of his swollen lower spinal cord. Myelography showed a filling defect and flow disturbance of contrast medium in lower thoracic levels, suggesting the presence of adhesive arachnoiditis. Spinal angiography demonstrated a fistula formation between dural branches of bilateral L4 lumbar arteries and ventral spinal and radicular veins on the surface of the dura mater of L4/5 levels. Considering his past history of repeated lumbar puncture for tuberculous meningitis at the age of 22 years, a diagnosis of acquired spinal dural arteriovenous fistula probably due to repeated lumbar puncture was made. Fistulas were embolized with N-butyl cyanoacrylate. And normal pressure hydrocephalus was treated by ventriculoperitoneal shunt. Follow-up CT scans showed a decrease of the size of the ventricular system. Etiology of acquired spinal arteriovenous fistula has been reported. In the case, repeated lumbar puncture may be a possible cause of arteriovenous fistula in the lower spinal dura mater. However, the reason why it took so long to form a fistula after the lumbar puncture remains to be elucidated. We suggest that an increased protein concentration due to disturbance of cerebrospinal fluid flow might be a cause of normal pressure hydrocephalus (NPH).

Arteriovenous Fistula↗
PubMed1995

Paralytic illness resembling inflammatory polyradiculoneuropathy in a chimpanzee.

An adult male chimpanzee housed in an outdoor corral with a group of other chimpanzees had an acute onset of ascending motor paresis that progressed to flaccid tetraplegia over 3 days. Tendon reflexes were weak, and CSF protein concentration was high. The chimpanzee regained normal mobility over several months. This chimpanzee's ascending, symmetrical, monophasic, flaccid paralytic illness, with albuminocytologic dissociation in CSF, and recovery following supportive treatment, was characteristic of inflammatory polyradiculoneuropathy, known as Guillain-Barré syndrome in human beings. Coonhound paralysis and experimentally induced allergic neuritis are the counterparts in dogs and laboratory animals, respectively, of the syndrome. In human beings, the syndrome is apparently immunologically mediated, as it is known to develop after bacterial and viral infections, vaccinations, and surgery or injury. The chimpanzee of this report had been given a rabies vaccination and had been treated for dental abscess 12 days prior to onset of signs, and had been inoculated with material containing neuronal antigens 20 years prior to onset of signs.

Animals↗
PubMed1995

[Neurological involvements with transient gait disturbance in subacute phase of Kawasaki disease; a case report].

A 1-year-and-9-months old boy with gait disturbance during the 3rd week of Kawasaki disease (KD) was described. He had been previously healthy, and developed high fever and rash. The diagnosis of KD was based on 5 of 6 major criteria on the 3rd clinical day. He was initially treated with intravenous gamma-globulin 400 mg/kg/day for five days. On the 17th clinical day, the patient developed gait disturbance after most clinical signs disappeared. His gait was wide- based and unstable. Generalized hypotonia with poor traction response was also seen. Pyramidal tract signs including exaggerated patellar and Achilles tendon reflexes and positive bilateral Mendel-Bechterew reflex were presented. Cerebrospinal fluid was normal. Brain CT, MRI, and 123I-IMP SPECT images were normal without broad hemorrhage or infarction of the cerebral parenchyma. Gait disturbance recovered spontaneously within one month without any sequelae.

Central Nervous System Diseases↗
PubMed1995

Friedreich's ataxia-vitamin E responsive type. The chromosome 8 locus.

The most common autosomal recessive ataxia is Friedreich's ataxia (FA), characterized mainly by an early onset, absent tendon reflexes, deep sensory loss, cerebellar and Babinski signs. Screening the patients from families with classical FA features, we found that some families were excluded from the FA locus on chromosome 9, and are associated to isolate vitamin E deficiency. The similarity of the clinical data between FA with and without vitamin E deficiency was remarkable. The disorder with vitamin E deficiency often confused with FA, is currently known as linked to chromosome 8q. Therefore it is important to test vitamin E levels in all patients suspected to have FA, since the alpha tocopherol supplementation may be efficient in early stages of the disease.

Child↗
PubMed1995

[A case of Guillain-Barré syndrome with ophthalmoplegia showing high titers of anti-GQ1b and -GD1b antibodies in the serum].

A 24-year-old housewife developed double vision, tingling sensation, and weakness in the legs following a flu-like illness. She then developed dysphagia and difficulty in standing. On admission her eyes were fixed in midline due to ophthalmoplegia. Doll's eye sign was negative. She had severe generalized muscle weakness and no sensory deficits. All tendon reflexes were lost. CSF protein was 58 mg/dl with cell count of 2/mm3. Antibodies to campylobacter jejuni, mycoplasma, EBV, and other microbes were negative. We treated her with plasmapheresis after which she showed rapid clinical recovery, although the ophthalmoplegia improved slightly later. Increased titer of IgG class antibodies to GD1b and to GQ1b, and of IgM antibody to GQ1b, were detected in the serum taken during the acute phase of the illness. In parallel with clinical amelioration, both the anti-GD1b and -GQ1b antibodies decreased in titer, or became negative. Since there is no common epitope to GD1b and GQ1b gangliosides, we speculated that the anti-GD1b and -GQ1b antibodies were induced independently by different antigens in this patient. Moreover, the presence of high titer IgM antibody to GQ1b possible indicates that this patient was at the relatively early stage of infection of unknown microbe, which then induced the IgG antibodies to GD1b and GQ1b by cross sensitization, which might correlate with the tetraplegia and the ophthalmoplegia, respectively.

Adult↗
PubMed1995

[A case of myokymia with abnormal F responses].

We reported a case of myokymia with abnormal F response. A 60-year-old male with chronic alcoholism was admitted to our hospital with complaint of muscle cramp in both legs just after drinking. Neurological examination revealed muscle pain and weakness of the legs, absence of bilateral Achilles tendon reflexes and prominent myokymia in his right quadriceps femoris and left calf muscles. The electrophysiological examination showed reduced conduction velocity, high amplitude, increased number of phases and long duration of F responses suggesting increased excitability of motoneuron pool. The epidural nerve block brought about a disappearance of the myokymia and an improvement of the abnormal features of F response. The myokymia gradually tended to be milder in the clinical course. The relationship between the myokymia and the abnormal F responses indicated that the increased excitability of spinal motoneurons might play an important role on the generation of myokymia of this patient.

Electromyography↗
PubMed1995

[A case of late-onset tethered cord syndrome presenting with spastic paraparesis].

We report a patient with late-onset tethered cord syndrome who presented with slowly progressive spastic paraparesis. Final diagnosis was made with spinal MRI. A 55-year-old man developed disturbance in gait at 52 years. He had severe congenital scoliosis of the thoracic spine and skin anomaly and hypertrichosis in the midline of the sacral region. His feet revealed pes equinovarus and pes cavus. Deep tendon reflexes in the lower extremities were hyperactive with positive Babinski signs. Vibration sense was diminished in the lower extremities. He had sexual impotence but no vesical or rectal disturbances. The plain X-rays revealed scoliosis at the fourth and fifth thoracic vertebrae, multiple costal fusion from the fourth through the eighth ribs on the left, and spina bifida occulta at the lumbosacral vertebrae. On MRI, the conus was tethered downward at the level between the forth and fifth vertebral bodies, and a thickened filum terminale connected the conus with a coccygeal cyst. Tethered cord syndrome, though rare in adults, should be differentiated from other diseases which produce late-onset spastic paraparesis, and MRI of the lumbo-sacral region is very useful for its diagnosis.

Age of Onset↗
PubMed1995

[Chronic inflammatory demyelinating polyneuropathy associated with chronic liver disease due to type B and type C hepatitis virus].

A patient with chronic inflammatory demyelinating polyneuropathy (CIDP) associated with type B and type C hepatitis virus infection is reported. A 54-year-old female who had a blood transfusion at the age of 31 years was diagnosed as a carrier of hepatitis B virus at the age of 43. Liver dysfunction was first noted in 1987 and gradually grew worse year by year. Beginning in early June 1992, the patients general fatigue became worse, her serum GOT and GPT levels became elevated, and she complained of a tingling sensation in her arms and legs. Neurological examination revealed moderate sensory disturbance of the glove-and-stocking type in all of her extremities. Deep tendon reflexes were all diminished. Hepatitis C antibody was detected in the serum at this time. On June 12, 1993, progression of her sensory disturbance was found to be associated with generalized muscle weakness. Cerebrospinal fluid studies showed increased protein without pleocytosis. Motor nerve conduction studies revealed marked prolongation of terminal latencies, reduction of conduction velocities, and abnormal temporal dispersion of the motor potentials. No sensory potentials could be evoked at any of the sites stimulated. Sural nerve biopsy showed segmental demyelination and severe loss of large myelinated fibers as well as some onion bulb formation. A diagnosis of CIDP was made. Treatment with corticosteroids was started, but there was little improvement in neurological function. The liver dysfunction progressed further and ultimately the patient died of hepatic failure. An autopsy demonstrated liver cirrhosis, but no malignant tumors were evident.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗
PubMed1994

[A case of acute pandysautonomia and diffuse brain stem impairment associated with EB virus infection].

A 37-year-old woman with complaints of headache and nausea presented with temporary disturbance of consciousness, bulbar palsy and ataxic speech following flu-like symptoms. After the recovery of her consciousness, she developed orthostatic syncope and numbness all over the body. When she was admitted to our hospital two months later, she showed emaciation, diminished sweat production and butterfly-patch-like pigmentation. Neurologic examinations were remarkable for anisocoric pupils that sluggishly reacted to light, impaired left facial movements, bulbar palsy, numbness of the whole body, total loss of all tendon reflexes, incordination, ataxic gait and severe postural hypotension. Laboratory data included albuminocytogenic dissociation in cerebrospinal fluid, convergence nystagmus and dysmetria in electronystagmography, and right trigeminal paralysis in blink reflex. A sural nerve biopsy showed active axonal degeneration and severe loss of both myelinated and unmyelinated fibers. Examinations of autonomic nervous system disclosed diffuse impairment of sympathetic and parasympathetic postganglionic nerve. Based on these findings she was diagnosed as having acute pandysautonomia. High titer of serum EB virus antibody suggested that acute pandysautonomia and diffuse brainstem impairment may be related to EB virus infection.

Acute Disease↗
PubMed1994

[A case of facioscapulohumeral muscular atrophy presenting unusual squatting gait, associated with tongue atrophy and sensorineural hearing loss].

A 16-year-old girl has presented speaking disturbance since early in life. Difficulty in running was noted at the age of 7. Her mother (46 years old) had moderate facial weakness and mild proximal weakness of the upper and lower limbs. Neurological examination at age 9 revealed bilateral facial weakness, tongue atrophy and weakness of the shoulder girdle, upper arms, and thighs. Deep tendon reflexes were absent in the four limbs. Gait was waddling. Over the next several years, she developed wasting and weakness around the shoulder girdle, upper arms, thighs, and increased lordosis. She lost the ability to walk by age 13. Since then, she has moved with difficulty in a squatting position. Serum CK was moderately increased and needle EMG in the extremities revealed myopathic changes. Muscle CT demonstrated marked atrophy of the proximal muscles in the left arm and lower limbs and mild atrophy of the calves. Audiogram showed bilateral mild sensorineural hearing loss. Muscle biopsy of the quadriceps at age 9 showed nondiagnostic findings. This case could be diagnosed as congenital facioscapulohumeral muscular dystrophy. Tongue atrophy and sensorineural hearing loss are rarely associated with this syndrome, as well as unusual squatting gait.

Adolescent↗
PubMed1995

[Surgical outcome of cervical flexion myelopathy in young adults].

We encountered five young male patients with cervical flexion myelopathy, and treated them all surgically. Symptoms were first noted at 15 to 18 years of age (mean: 16.6 years), and their ages at the time of admission to our hospital, ranged from 19 to 25 years old (mean: 20.8 years). Anterior decompression and fusion of the cervical spine with long bone graft following resection of two vertebrae was performed in three cases. The other two patients were treated by posterior fusion of five laminas (C3-C7) using Rogers' method. In selecting the surgical approach, we favored anterior fusion because it allows removal of anterior structures (vertebral bodies, intervertebral discs or osteophytes) compressing the cervical spinal cord in flexed neck position. Posterior fusion was performed in patients whose anterior structures compressing the cervical spinal cord extended over a wide area. Postoperative improvement of muscle weakness was observed in four patients, and sensory disturbance was alleviated in the remaining patient. However, the abnormal deep tendon reflexes and muscle atrophy in the upper extremities observed in all of the patients preoperatively improved in only two of them. Thus, all of the patients showed some neurological improvement, and surgical fusion of the cervical spine appeared to be an effective means of treating cervical flexion myelopathy in young adults. Both the anterior and the posterior approach were useful in treating cervical flexion myelopathy, but it was impossible to conclude which approach is more effective based on this small number of cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[A 65-year-old woman with dysarthria, dysphagia, weakness, and gait disturbance].

We report a 65-year-old woman with progressive dysarthria, dysphagia, weakness, and gait disturbance. The patient was well until 59 years of age (January of 1986) when she noted bilateral ptosis. One year later, she noted a gradual onset of difficulty in speech (articulation). Her speech slowly deteriorated and she noted weakness in chewing power and difficulty in swallowing in addition. In October 1987, she developed emotional incontinence. In January of 1988, she started to drag her left foot. She was admitted to our hospital on June 13 of 1988. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed no dementia; her higher cerebral functions appeared intact. Ptosis was present bilaterally more on the right. She showed difficulty in opening her eyes on command; no contraction of the frontal muscles was seen upon attempted eye opening. There was a moderate limitation in the vertical gaze. Forced laughing and crying were seen. Facial muscles were moderately weak without apparent atrophy. The movement of the soft palate was very weak, and swallowing disturbance was more prominent for liquid staff. The tongue appeared somewhat small, however, no fasciculation was noted. Her step was small and the posture was stooped. Retropulsion was present, however, Romberg's sign was absent. No muscle atrophy was apparent, however, diffuse mile to moderate muscle weakness was noted in all four limbs. Cerebellar sign was absent. Deep tendon reflexes were exaggerated bilaterally, and Babinski sign was present on the left side. Sensation was intact. Routine blood tests were unremarkable as was a cranial CT scan. Her ptosis did not improve after 10 mg of edrophonium injection. CSF was also normal. She was transferred to another hospital but her neurological disabilities further progressed. In 1989, she was totally unable to move her limbs; she could only move her eyes; still consciousness was clear without dementia. She developed respiratory difficulty and expired on July 25, 1992. She was discussed in a neurological CPC, and the opinions were divided into ALS and primary lateral sclerosis (PLS). The chief discussant arrived at the conclusion that the patient might have had the pyramidal form of ALS. Postmorten examination revealed marked myelin pallor in the anterior as well as lateral corticospinal tracts. Pyramidal tract degeneration was prominent starting at the level of the cerebral peduncle and was continued to be seen until the level of lumbar cord. The number of anterior horn cells showed only slight decrease in the cervical level, however, it was normal in the lumbar cord.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1995

[A case of localized hypertrophic neuropathy in the sciatic nerve].

A 26-year-old male patient gradually developed muscular atrophy of the right lower leg over a two-year period. Neurological examination revealed absent Achilles tendon reflex and muscular atrophy of the right lower leg and right hamstring muscles. Conduction velocity of the F waves was delayed in the right posterior tibial nerve. A computerized tomography scan and magnetic resonance imaging revealed a mass lesion along the proximal segment of the right sciatic nerve. Exploration revealed a fusiformly swollen sciatic nerve. Histological examination showed that a swollen segment of the sciatic nerve was filled with onion-bulb formations of perineurial cells, consistent with the diagnosis of localized hypertrophic neuropathy. This condition should be added to several etiologies of monomelic amyotrophy. Electrophysiological studies and neuroimaging techniques were useful in obtaining differential diagnosis.

Adult↗
PubMed1995

[Siblings of early onset cerebellar ataxia with hypoalbuminemia].

Recently, a new syndrome of early onset cerebellar ataxia with hypoalbuminemia (EOCA-HA) was reported in Japan. The clinical features of EOCA-HA overlap with those of Friedreich's ataxia (FA), and primary hypoalbuminemia is a characteristic laboratory finding of this syndrome. Genetic linkage analysis of EOCA-HA including this newly reported family revealed that the gene for EOCA-HA is located on the long arm of chromosome 9 as FA. However, several recombination events were observed between D9S15 in EOCA-HA, whereas no recombination events were seen in FA. We report on two siblings with EOCA-HA and discuss the clinical and laboratory features. The patients were a 25-year-old man (patient 1) and a 23-year-old man (patient 2). Their parents marriage was non-consanguineous. The mode of inheritance is compatible with autosomal recessive mode. Clinically, they showed cerebellar ataxia as the initial symptom in the late infantile period and subsequently showed choreoathetosis and ocular motor apraxia at the age of approximately fifteen years. Deep tendon reflexes were reduced in late infancy and finally disappeared. Amyotrophy and sensory impairment of the legs developed at approximately twenty. Abnormal electrocardiogram and diabetes mellitus were not observed. On X-ray CT scan or MRI, the cerebella of both patients were mildly atrophic. Clinical features in these siblings were indistinguishable from those of ataxia telangiectasia, but immunodeficiency syndrome was absent.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Development of Wernicke's encephalopathy during the period of oral food intake after a subtotal colectomy for ulcerative colitis].

A 61-year-old woman was hospitalized because of ulcerative colitis which had caused fever, vomiting and diarrhea since June 16, 1992. Then she developed toxic megacolon, and was transferred to our hospital on the 1st of July and underwent subtotal colectomy the same day. After surgery, she received intravenous hyperalimentation (IVH) which contained 1,000 Kcal/day without vitamin supplementation. From the 8th to the 13th post-operative days, she took 3/4 or more of the liquid diet which contained 1,050 Kcal, protein 35 g, carbohydrate 166 g and vitamin B1 0.59 mg per day. From the 14th to the 23rd post-operative days, she ate 4/5 or more of the oral diet which contained 1,700 Kcal/day, protein 68 g, carbohydrate 236 g and vitamin B1 0.93 mg per day. During the 7th to the 23rd day, the IVH was reduced to 800 Kcal and then 500 Kcal per day. She talked less on the 19th post-operative day, and in a few days, her level of consciousness began to decline progressively. On the 27th post-operative day, neurological examinations revealed the following: semi-coma, almost fixed pupils which were 3 mm in diameter, absent doll's eye movement to all directions, flaccid extremities with abolished deep tendon reflexes. Pertinent abnormalities on laboratory data at that time consisted of hemoglobin 7.8 g/dl and serum total protein 5.4 g/dl. Lumbar puncture revealed normal cerebrospinal fluid under normal opening pressure. Cranial magnetic resonance imaging (MRI) taken on the 27th post-operative day demonstrated, on T2-weighted images, symmetrical high intensity lesions in the periventricular areas of the third and fourth ventricles, and periaqueductal area of the midbrain.(ABSTRACT TRUNCATED AT 250 WORDS)

Colectomy↗
PubMed1995

[Complete deficiency of adhalin (50 kDa DAG) in skeletal muscle of malignant limb-girdle muscular dystrophy].

Malignant limb-girdle muscular dystrophy was first described by Miyoshi and co-workers in 1966, and has clinical features similar to Duchenne muscular dystrophy but is inherited through an autosomal recessive trait. This paper describes a patient with malignant limb-girdle muscular dystrophy with complete deficiency of adhalin (50 kDa dystrophin-associated glycoprotein (DAG)) in skeletal muscle. The patient was an 11-year-old Japanese girl whose parents were cousin. She learned to walk at one year and 3 months of age. Her gait became unsteady at 3 years of age, and motor dysfunction in the lower extremities progressed thereafter. At 8 years of age, she had difficulty in standing up from a sitting position, but could walk without assistance. At 11 years, she could walk with support, but could not stand up without assistance. Her intelligence was normal. Muscle atrophy was not apparent due to obesity, but her calves appeared hypertrophic. She had generalized muscle weakness, predominantly in the pelvic girdle muscle. Muscle tone was slightly hypotonic, and deep tendon reflexes of the legs were absent or hypoactive. Her sensory system appeared normal. Serum creatine kinase level was elevated to 30 times above the upper limit of the normal range in the patient and normal in her parents. EMG showed a mild myopathic pattern. CT scan of muscle revealed marked low density in the upper legs and mild in the lower legs. Muscle histology showed muscle fiber necrosis with a small number of regenerating fibers. Opaque fibers were occasionally observed, but not as many as in Duchenne type. Fiber splitting was seen frequently.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1995

[HTLV-I-associated neuropathy].

A 70-year-old man was admitted to our hospital because of a 15-year history of walking difficulty, disturbance of sensation in the palm for 2 years and hand tremor for 6 months. On admission, the scapulohumeral muscles showed fasciculation and atrophy. There was action tremor in the upper limb, and the proximal lower limb showed atrophy and weakness. Standing and walking were impossible. Deep tendon reflexes were decreased in lower limbs. Pathologic reflexes were not found. There was distal dominant sensory disturbance, and urination was difficult. Needle EMG showed a neurogenic pattern in 4 all limbs. MCV and F-latency were delayed. SCV in the median nerve and the amplitude in the sural nerve were decreased. Biopsy of the sural nerve revealed both axonal change and demyelination. Biopsy of the quadriceps femoris muscle showed neurogenic change with helper T-cell infiltration. Anti-HTLV-I antibody and ATL-like cells in both blood and CSF were positive. There were HTLV-I provirus DNA with a polyclonal pattern and the type of HLA as HAM. The HTLV-I infection was of the HAM type. As the present patient showed mainly neuropathy without pyramidal signs, was not considered to have HAM.

Aged↗
PubMed1994

Magnesium and therapeutics.

Two different types of therapy with magnesium are used: physiological oral magnesium supplementation which is totally atoxic since it palliates magnesium deficiencies by simply normalizing the magnesium intake and pharmacological magnesium therapy which may induce toxicity since it creates iatrogenic magnesium overload. Primary and secondary magnesium deficiencies constitute the sole indication of physiological oral magnesium therapy. It is therefore necessary to be well acquainted with the clinical and paraclinical pattern of magnesium deficit and to discriminate between magnesium deficiency due to an insufficient magnesium intake which only requires oral physiological supplementation and magnesium depletion related to a dysregulation of the control mechanisms of magnesium status which requires more or less specific regulation of its causal dysregulation. Physiological oral magnesium load constitutes the best tool for diagnosis of magnesium deficiency and the first step of its treatment. Physiological oral magnesium supplementation (5 mg/kg/day) is easy and can be carried out in the diet or with magnesium salts, with practically only one contra-indication: overt renal failure. Specific and aspecific treatments of magnesium depletion are tricky using for example magnesium sparing diuretics, pharmacological doses of vitamin B6, physiological doses of vitamin D and of selenium. In order to use the pharmacological properties of induced therapeutic hypermagnesaemia, high oral doses of magnesium (> 10 mg/kg/day) are advisable for chronic indications and the parenteral route is suitable for acute indications. There are 3 types of indications: specific (for the treatment of some forms of magnesium deficit i.e. acute), pharmacological (i.e. without alterations of magnesium status) and mixed--pharmacological and aetiopathogenic--(for example complications of chronic alcoholism). Today pharmacological magnesium therapy mainly concerns the obstetrical, cardiological and anaesthesiological fields. The main indications are eclampsia, some dysrhythmias (torsades de pointe particularly) and myocardial ischaemias. But it is now difficult to situate the exact place of the pharmacological indications of magnesium. Magnesium infusions can only be envisaged in intensive care units with careful monitoring of pulse, arterial pressure, deep tendon reflexes, hourly diuresis, electrocardiogram and respiratory recordings. High oral magnesium doses besides their laxative action may bring latent complications which may reduce lifespan. There may remain some indications of the laxative and antacid properties of non soluble magnesium, particularly during intermittent haemodialysis. Lastly local use of the mucocutaneous and cytoprotective properties of magnesium is still valid, in cardioplegic solutions and for preservation of transplants particularly.

Administration, Oral↗