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PubMed1996

[Distal spinal muscular atrophy].

Chronic spinal muscular atrophy usually presents in childhood or adolescence, generally as predominant proximal muscle weakness. Other less common forms involving distal muscles can be either partial or generalized and their prognosis is relatively good. At least three well-defined types can be identified: a) a form located in the upper extremities that typically affects young men, is not familial and is highly prevalent in Asia; b) a more generalized form that can be either familial or isolated and that resembles Charcot-Marie-Tooth disease in the distribution of muscle weakness and prognosis, and c) another generalized form that starts in and mainly involves the upper extremities, is inherited in an autosomal dominant manner and is accompanied by laryngeal involvement. We review the literature and describe 27 patients with distal spinal muscular atrophy resembling Charcot-Marie-Tooth disease.

Adolescent↗

PubMed1994

Respiratory effort perception at rest and during carbon dioxide rebreathing in patients with dystrophia myotonica.

BACKGROUND: Breathlessness appears to be closely related to the perception of the outgoing motor command to breathe and should be increased in the presence of muscle weakness. However, breathlessness is not a common symptom in patients with chronic muscle disease who have weak respiratory muscles. The factors that determine the perception of respiratory effort in such patients have not been examined. METHODS: The inspiratory effort sensation during resting breathing and progressive hypercapnia was investigated in 12 patients with dystrophia myotonica with weak respiratory muscles (nine men and three women of mean (SD) age 41.1 (10.5) years; maximum inspiratory pressure 43.1 (17.2) cm H2O) and an age and sex matched control group of normal subjects of mean age 39.6 (10.6) years and a maximum inspiratory pressure of 123 (15.2) cm H2O. RESULTS: During resting breathing with a mouthpiece no differences were seen in inspiratory effort sensation, mouth occlusion pressure, or tidal volume, but inspiratory time and cycle duration were significantly shorter in the patients with dystrophia. Minute ventilation (VE) was significantly higher in the patients (15.8 (4.0) l/min v 12.5 (2.6) l/min), while resting breathing was no more variable in the patients than in controls. The ventilatory response to carbon dioxide (VE/PCO2) was not significantly lower in the patients (14.9 (6.9) l/min/kPa) than in the controls (17.4 (4.3) l/min/kPa). Effort sensation responses to carbon dioxide driven breathing were similar in the control subjects and the patients. With regression analysis of pooled data neither maximum inspiratory pressure nor disease state contributed to perceived inspiratory effort during hypercapnia. CONCLUSIONS: Moderately severe global respiratory muscle weakness does not appear to influence the ventilatory response to rising carbon dioxide tension or the perception of inspiratory effort in patients with dystrophia myotonica.

Adult↗

PubMed2001

MRI guided muscle biopsy confirmed polymyositis diagnosis in a patient with interstitial lung disease.

UNLABELLED: Idiopathic inflammatory myopathies, such as polymyositis (PM), may present with general symptoms such as fever and fatigue and only minimal muscle weakness, making it difficult to make a definite diagnosis and provide adequate treatment. Here a case is described in which interstitial lung disease was the first and most prominent manifestation of PM. Later, when muscle weakness became apparent and inflammatory muscle disease was suspected the first muscle biopsy was non-diagnostic. However, magnetic resonance imaging (MRI) scans of the clinically weak thigh muscles showed high signal on T(2) weighted images, suggesting muscle inflammation more proximal to the first biopsy site. A second biopsy at this site disclosed typical histopathological findings for myositis. After treatment with prednisolone in combination with cyclophosphamide both pulmonary and muscle function improved. CONCLUSION: MRI scans of muscles may be helpful in selection of a site for muscle biopsy in patients with suspected inflammatory myopathy when a first muscle biopsy turns out to be negative. Additionally, patients with interstitial lung disease of unknown cause should be tested for muscular function to exclude an associated inflammatory muscle disorder.

Anti-Inflammatory Agents↗

PubMed2005

Understanding critical illness myopathy: approaching the pathomechanism.

Myopathies occurring in critically ill patients have gained increasing interest during the past years. For the patient, they represent a crucial factor for prolonged intensive care unit treatment and secondary complications. Critical illness myopathies (CIMs) seem to be related to various pathogenic factors. Among those, the septic inflammatory response syndrome seems to play a major role. It has been suggested that, similar to sepsis-related multiorgan failure, CIM might be considered a failure of the organ muscle. Muscle function might be impaired by proposed "myotoxic" humoral factors. These could be endogenously produced during the innate immune response to sepsis. This article follows up recent evidence for such active fractions in the blood serum of CIM patients. To explain muscle weakness in CIM, serum fractions acutely modified membrane excitability and subcellular Ca2+ regulation in an animal model. From the differential serum effects, early-phase CIM seems to involve a reduction in the overall force generation in muscle but also a compensation by the membrane, increasing the excitability. Different animal models will help to elucidate the underlying mechanisms accounting for the specific proteolytic activities found in different forms of CIM. CIM represents a systemic rather than a local disorder. Humoral factors might initiate the local reaction of skeletal muscle clinically seen as muscle weakness, altered excitability, and proteolysis of contractile proteins. Establishing the interactions in the excitation-contraction cascade in CIM is a challenging task, not only to clarify its pathomechanism but also to deduce clinical interventions.

Animals↗

PubMed2003

[A case of anaphylactoid shock occurring immediately after the initiation of second intravenous administration of high-dose immunoglobulin (IVIg) in a patient with Crow-Fukase syndrome].

We report a case of anaphylactoid shock occurring immediately after the initiation of second intravenous administration of high-dose immunoglobulin (IVIg) in a patient with Crow-Fukase syndrome. The patient was a 57-year-old woman, who was admitted to our hospital because of numbness and muscle weakness in the four extremities, difficulty in walking, and foot edema. On admission, her skin was dry and rough, and also showing scattered pigmentation, small hemangiomas, and hypertrichosis in both legs. She had distal dominant muscle weakness, more prominent in her legs, and was not able to walk. Deep tendon reflexes in her four extremities were markedly diminished or absent. She had a glove and stocking type of paresthesia, severe impairment of vibration, and absence of joint position sensation in her four extremities. On laboratory data, serum vascular endothelial growth factor (VEGF) was markedly elevated to 5,184 pg/ml (normal: below 220 pg/ml). Cerebrospinal fluid examination revealed cell counts of 2/microliter and protein level of 114 mg/dl. Abdominal echo showed marked hepatosplenomegaly. On peripheral nerve conduction study, both motor and sensory conduction velocity were undetectable in her legs. We diagnosed her condition as Crow-Fukase syndrome, and started IVIg of polyethyleneglycol-treated gamma-globulin (PEG-glob) at 400 mg/kg/day for 5 consecutive days for polyneuropathy. Since the first IVIg mildly improved muscle weakness, we tried the second IVIg of PEG-glob. However, immediately after the initiation of second IVIg of PEG-glob, she developed hypotention, dyspnea, cold sweating, cyanosis, and became lethargic. We immediately stopped IVIg and started first-aid treatment with epinephrine and corticosteroid for these symptoms. This treatment was successful and the patient fully recovered without any sequelae. Since serum IgE level remained unchanged and lymphocyte stimulation test (LST) was positive against the same rot number of PEG-glob, we diagnosed these symptoms as anaphylactoid shock. Based on the results of LST, we speculated that PEG-glob was the causative agent of anaphylactoid reaction. Anaphylactic or anaphylactoid reaction as adverse effects of IVIg is very rare, and to our knowledge, there are only 4 previous reports of anaphylactic or anaphylactoid reaction caused by IVIg. Therefore, we speculated that the prominent high level of serum VEGF in the present patient might play a significant contributory role in the development of anaphylactoid shock, since the vascular permeability of VEGF is 50,000 times stronger than that of histamine. We consider that it is necessary to carefully monitor IVIg of PEG-glob administration for polyneuropathy in patients with high level of serum VEGF, like Crow-Fukase syndrome.

Anaphylaxis↗

PubMedDate not supplied

[Acquired neuromuscular syndrome in critically ill patients].

AIMS: To analyse the causes and signs of the muscle weakness that critically ill patients develop during their stay in the ICU and to review the literature. DEVELOPMENT: In the early 80s, Bolton reported a mixed axonal polyneuropathy that he called 'polyneuropathy in critically ill patients'. Clinically it was characterised by muscle weakness that varied in intensity and caused quadriplegia and/or the need for assisted ventilation in its severest forms. It is currently considered to be the most common neurological disorder among critically ill patients. Many patients made a complete recovery after a few months or even a year. Running almost parallel to this, he also described 'acute myopathy in intensive care' among asthmatic patients who were hospitalised in the ICU due to exacerbation of their illness. It was later observed how other types of patients also had this myopathy, for instance, those who had undergone a transplant, sepsis or burns. Some authors consider acute myopathy in intensive care to be the primary cause of muscle weakness in the ICU. CONCLUSIONS: On many occasions 'polyneuropathy of critically ill patients' and 'acute myopathy in intensive care' can be differentiated and to do so neurophysiological and, if necessary, muscle biopsy studies are a valuable aid. Although some authors prefer to group these conditions under the name 'polyneuromyopathy', we propose the general term 'acquired neuromuscular syndrome in critically ill patients' -a more descriptive expression that does not presuppose a particular mechanism or a single aetiology.

Critical Illness↗

PubMed2006

[A case of cervical spondylotic amyotrophy resembling post-polio syndrome].

We reported a 62-year-old man with cervical spondylotic amyotrophy, in whom differentiation from post-polio syndrome was required. At the age of 3, the patient developed acute anterior poliomyelitis that caused muscular atrophy and muscle weakness in the left arm and bilateral lower limbs. At the age of 61, after approximately 58 years of symptomatic stabilization, the patient newly developed muscular atrophy and muscle weakness localized in the triceps muscle of the left arm. Since no sensory disturbance was noted, post-polio syndrome was initially suspected. However, MRI and myelo-CT demonstrated left side compression of the spinal cord at the level of the 6th cervical spine. Therefore, the patient was diagnosed as having cervical spondylotic amyotrophy, and the progression of the disease was prevented by having the patient rest. Since this patient had a history of acute anterior poliomyelitis, the number of anterior horn cells might have been decreased before he developed cervical spondylosis. Therefore, the patient might have shown clinical symptoms of cervical spondylotic amyotrophy mainly consisting of anterior horn disturbance and scarce sensory disturbance.

Cervical Vertebrae↗

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↗

PubMed2000

Combination thyroplasty and the "twisted larynx:" combined type IV and type I thyroplasty for superior laryngeal nerve weakness.

Vocal cord medialization through Isshiki type I thyroplasty is part of the standard approach for patients with unilateral vocal cord immobility secondary to recurrent laryngeal nerve paralysis. However, several other modalities have been used to treat the symptomatic "twisted" larynx caused by unilateral superior laryngeal nerve weakness. The Isshiki type IV thyroplasty (cricothyroid approximation) specifically addresses cricothyroid muscle weakness, but, canine studies at the Mayo Clinic demonstrated a trend toward decreased acoustic power and sound intensity with simulated cricothyroid activity. Thus it is reasoned that addition of an ipsilateral type I thyroplasty should help compensate for this power loss. Using videostroboscopic and acoustic analysis, 9 patients with unilateral superor laryngeal nerve weakness were treated with combination type IV and type I thyroplasty. Subjective dysphonia and objective visual and acoustic measurements revealed postoperative improvement in most patients. The combination type IV and type I thyroplasty is recommended for surgical treatment of patients with superior laryngeal nerve weakness, because it addresses cricothyroid muscle weakness without compromising vocal power.

Adult↗

PubMed1995

[Polymyositis with rimmed vacuoles in a case of chronic thyroiditis].

We report a 37-year-old woman who developed chronic thyroiditis, and polymyositis with rimmed vacuoles (RVs). She developed paresthesia of glove and stocking type, muscle weakness of the lower extremities, and slowness in motion. On examination, her lower legs were atrophic and weak, more prominent on the right, while proximal muscles in the upper and lower extremities were slightly affected. Deep tendon reflexes of the upper and lower extremities were normal except for the absent Achilles tendon reflexes. Serum CK was high (1,809 IU/l), and laboratory data indicated chronic thyroiditis and hypothyroidism. Muscle CT showed severe fatty changes in the gastrocnemius and soleus muscles, more marked on the right, and slight atrophy of the thigh muscles. Electromyography and nerve conduction velocity study revealed peripheral neuropathy. Muscle biopsy revealed numerous myofibers with RVs, together with myofiber necrosis, phagocytosis and lymphocyte infiltration, consistent with myositis. Nerve biopsy was indicative of slight axonal degeneration. A diagnosis of polymyositis with RVs in combination with chronic thyroiditis was made. Prednisolone combined with levothyroxine markedly improved muscle weakness though atrophy and weakness of the lower legs were barely improved. Distal-dominant asymmetric affection of the leg muscles and many myofibers with RV on the biopsied muscle are atypical and rare findings of polymyositis. Associated chronic thyroiditis and neuropathy may be related to the formation of marked rimmed-vacuolar degeneration of myofibers in the present case.

Adult↗

PubMed2003

West Nile virus infection in 2002: morbidity and mortality among patients admitted to hospital in southcentral Ontario.

BACKGROUND: In August and September 2002 an outbreak of West Nile virus (WNV) infection occurred in southern Ontario. We encountered a number of seriously ill patients at our hospitals. In this article we document the clinical characteristics of these cases. METHODS: We conducted a retrospective chart review of patients who came to the attention of infectious disease or neurology consultants or the microbiology laboratories at 7 hospitals in the municipalities of Toronto, Peel and Halton, Ont. Patients were included if they had been admitted to hospital or stayed overnight in the emergency department, had serological evidence of WNV infection and had clinical evidence of WNV fever, aseptic meningitis, encephalomyelitis or motor neuronopathy. RESULTS: In all, 64 patients met the inclusion criteria; 57 had encephalitis or neuromuscular weakness or both, 5 had aseptic meningitis, and 2 had WNV fever. The mean age was 61 years (range 26-87). The patients were predominantly active, middle-aged or elderly people living independently in the community. Seven patients were immunocompromised A febrile prodromal illness preceded the neurological symptoms in almost all cases. The most common neurological abnormality was decreased level of consciousness; this frequently evolved to severe lower motor neuron neuromuscular weakness. Ataxia and swallowing disorders were frequent and important problems. Sixteen patients (25%) required intubation and mechanical ventilation because of a decreased level of consciousness, inability to clear secretions or respiratory muscle weakness; 9 others had disabling muscle weakness of one or more limbs. Ten patients died. The study patients were in hospital a total of 1856 patient-days, including 532 patient-days in an intensive care unit. Only 28% (13/47) of the patients who survived encephalitis or neuromuscular weakness, or both, were discharged home without additional support. Slow turnaround time for serological test results resulted in delayed diagnosis. INTERPRETATION: The 2002 WNV infection outbreak in Ontario caused serious morbidity and mortality in the subset of patients who had encephalitis or neuromuscular weakness severe enough to require hospital admission.

Adult↗

PubMed1981

Syndromes of toluene sniffing in adults.

Clinical and laboratory findings in 25 adults, ages ranging from 18 to 40 years, who were hospitalized for problems related to paint sniffing are presented. All but one were chronically unemployed. Three different patterns of symptoms led to hospitalization: muscle weakness (n = 9), gastrointestinal complaints including abdominal pain and hematemesis (n = 6) and neuropsychiatric disorders including altered mental status, cerebellar abnormalities, and peripheral neuropathy (n = 10). Hypokalemia (n = 13), hypophosphatemia (n = 10), hyperchloremia (n = 22), and hypobicarbonatemia (n = 23) were common. The average serum potassium and phosphorus concentrations of 1.7 mmol/L and 1.5 mg/dL were significantly lower in the muscle weakness group than in the other two groups. Rhabdomyolysis occurred in 10 patients. Hyperchloremic acidosis was found in 19 of 22 patients evaluated. The muscle weakness and gastrointestinal syndromes resolved within 1 to 3 days with abstinence from sniffing and repletion of fluid and electrolyte stores. Inhalation of paint or glue vapors should be considered in the differential diagnosis of the symptoms and laboratory findings described above.

Adolescent↗

PubMed1989

Neurologic manifestations of fluid and electrolyte disturbances.

The schema in Table 1 illustrates the inter-relationship between the major fluid and electrolyte disturbances with their primary site of involvement, that is, the CNS or peripheral nervous system (PNS), their primary effect (nervous system depression or irritability), and the major symptom complex associated with these sites and mechanisms (obtundation, seizures, muscle weakness, and tetany). As can be seen, a pattern emerges. Disorders of sodium and osmolality, whether hypernatremia (hyperNa), hyponatremia (hypoNa), hyperosmolality (hyperOsm), or hypo-osmolality (hypoOsm), all produce CNS depression with encephalopathy as the major clinical manifestation. Disorders of potassium, whether hyperkalemia (hyperK) or hypokalemia (hypoK), produce PNS depression with muscle weakness as the major clinical manifestation. On the other hand, disorders of magnesium and calcemia produce both CNS and PNS manifestations. Hypercalcemia (hyperCa) and hypermagnesemia (hyperMg) produce CNS and PNS depression with encephalopathy and muscle weakness, respectively, being the major clinical manifestations. Hypocalcemia (hypoCa) and hypomagnesemia (hypoMg) produce CNS and PNS irritability with seizures and tetany, respectively, being the major clinical manifestations.

Cations↗

PubMed2003

Myalgia as the revealing symptom of multicore disease and fibre type disproportion myopathy.

BACKGROUND: Multicore disease and congenital fibre type disproportion myopathy are diseases assigned to the heterogeneous group of congenital myopathies. Although hypotonia and muscle weakness appearing in early life are the commonest manifestations of these diseases, distinct phenotypes and late onset cases have been described. OBJECTIVE: To report the occurrence of myalgia as the revealing symptom of multicore disease and fibre type disproportion myopathy. METHODS: The clinical cases of three patients with fibre type disproportion myopathy and one with multicore disease are described. Skeletal muscle biopsies were processed for routine histological and histochemical studies. RESULTS: The clinical picture was unusual in that the symptoms were of late onset and the predominant complaint was muscle pain exacerbated by exercise. Muscle weakness was found in only a single patient, the mother of a patient with fibre type disproportion myopathy. Physical examination was unremarkable in the other patients. Muscle biopsies from patients 1 and 2 contained type I fibres that were considerably smaller than the type II fibres, supporting the diagnosis of fibre type disproportion myopathy. Skeletal muscle of patient 4 showed multiple areas, predominantly but not exclusively in the type I fibres, from which oxidative enzyme activities were absent, as seen in multicore disease. CONCLUSIONS: Muscle pain was the main clinical manifestation in our patients. Recognition of the broader clinical expression of these myopathies is important for prognostic reasons and for genetic counselling of the family members.

Adolescent↗

PubMed2005

Non-invasive Mechanical Ventilation Enhances Patient Autonomy in Decision-Making Regarding Chronic Ventilation.

OBJECTIVE: Patients with respiratory failure due to progressive muscle weakness often require chronic ventilatory support, but many do not make decisions regarding ventilation prior to a crisis. We studied the use of non-invasive ventilation as a tool to enable communication and facilitate decision-making regarding chronic ventilation. METHODS: Patients with profound muscle weakness and acute respiratory failure, were supported or weaned by non-invasive positive or negative pressure ventilation. The patients were then interviewed and their informed autonomous decisions were used to plan their future management. RESULTS: Non-invasive ventilation could be used safely to support patients with acute respiratory failure until decisions regarding chronic ventilation are made and as an alternative means of ventilation for those who refuse tracheostomy. CONCLUSIONS: Non-invasive ventilation may be used in patients with profound muscle weakness, as a means of enhancing patient autonomy by improving communication and maintaining ventilation until decisions about ongoing care are made.

Journal Article↗

PubMed1995

How to design a therapeutic study in patients with the post-polio syndrome. Methodological concerns and status of present therapies.

The innervation of muscles in patients with the post-polio syndrome (PPS) may differ from limb to limb or even within the same limb because of the segmental nature of the initial involvement and the varying degree of subsequent recovery. Consequently, the compensatory effort of the neighboring muscles varies even in the same limb. Clinicohistological studies have confirmed that in PPS the various muscle groups differ according to whether they were affected during the acute polio and have recovered (partially or completely), or whether they were clinically spared during the original disease, in spite of subclinical involvement. Because the impact of the late effects of polio is also variable in these muscle groups, the effect of therapies may be different not only from patient to patient and from limb to limb, but also from muscle to muscle within the same limb. These variables require careful statistical determination of the sample size at the design of a trial. Another problematic issue in the therapy of PPS is to define the end point of therapy. The two disabling PPS symptoms, excessive fatigue and new muscle weakness, can coexist. An experimental therapeutic design must focus separately on the fatigue, using validated fatigue scales, and on muscle weakness, using quantitative muscle testing. Another methodological concern is the placebo-controlled design. Patients with PPS, even those without depression, can be prone to a placebo effect; hence the need for controlled trials. Finally, the length of a trial remains unresolved because of the slow and unpredictable progression of PPS that varies from patient to patient. Until the natural history of PPS is defined, therapies aimed at arresting disease progression are not reliable.

Controlled Clinical Trials as Topic↗

PubMed1997

Oculopharyngeal muscular dystrophy in Italy.

Oculopharyngeal muscular dystrophy (OPMD) is an autosomal dominant myopathy particularly frequent in Québec. The few Italian cases thus far described with bilateral ptosis, dysphagia and variable muscle weakness, show non-specific dystrophic findings on muscle biopsies by light microscopy. We describe a 70-year-old Italian woman with an adult-onset ptosis, mild dysphagia and proximal muscle weakness belonging to a family segregating OPMD according to an autosomal dominant mode of inheritance. Clinical features of four of her relatives are reviewed. Muscle biopsy studied by electron microscopy showed the typical 8.5 nm in diameter intranuclear filamentous inclusions (INI). To our knowledge, this is the first Italian report of OPMD with INI. The identification of nuclear inclusions is mandatory in order to confirm the diagnosis prior to linkage analysis.

Aged↗

PubMed1996

[Polymyositis followed by myasthenia gravis].

A 63-year-old woman was admitted to the hospital because of swelling of both forearms and muscle weakness in the limbs. Laboratory examination revealed abnormally high levels of serum creatine kinase, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, and lactate dehydrogenase. Polymyositis was diagnosed, and prednisolone was administered. Her condition had been well controlled on prednisolone until several months before admission, when bilateral blepharoptosis and diplopia developed. An edrophonium test was positive: muscle weakness was transiently alleviated. High titers of anti-acetylcholine receptor antibodies were found. A chest CT scan showed a mass in the anterior part of the mediastinum. We diagnosed myasthenia gravis associated with thymoma. After an extended thymectomy, the patient's condition improved. When muscle weakness recurs after remission of polymyositis, myasthenia gravis should be considered.

Anti-Inflammatory Agents↗