Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “REFLEX, TENDON”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,369 records · Page 76Linked to original sources
PubMed2007

[A case of Möbius syndrome presenting with symptoms of severe infantile form of congenital muscular disorder].

Möbius syndrome is a rare disorder characterized by congenital bilateral facial nerve palsy. Abducent palsy or other cranial nerve palsy, facial malformations, limb malformations, and skeletal malformations are common features associated with this syndrome. We report a 9-month-old infant in whom congenital muscular disorder was previously suspected because of facial muscle involvement (mask-like face), respiratory and swallowing disturbances, and hypotonia since birth. After an improvement in the respiratory infection, she showed slightly exaggerated deep tendon reflexes and an improvement in muscle tone. The occurrence of combined facial nerve palsy, glossopharyngeal nerve palsy, vagus nerve palsy, and hypoglossal nerve palsy strongly suggested that she had Möbius syndrome. Finally, the absence of the roots of bilateral facial nerves on an MRI confirmed that the disorder was Möbius syndrome. We propose that a thin slice MRI should be obtained to observe the cranial nerves around the brain stem if patients show symptoms of congenital myopathy or congenital myotonic dystrophy as well as facial nerve and other cranial nerve paralyses.

Brain Stem↗
PubMed1990

Clinical, laboratory and immunologic effects of the treatment of endemic goiter with T4, T3 and KI.

We treated 204 patients with endemic nontoxic goiter with T4, T3 and KI, singly or in combination. Definitely nodular goiters were excluded, since the possibility of autonomy would be increased. Goiter size was evaluated before and 6 months after treatment clinically in a blind way, i.e. the observer (always the same) did not know either the pretreatment goiter size or the treatment the patient had received. At the same time various laboratory parameters were recorded. All the active treatments (but not placebo) resulted in a highly significant decrease in the gland size. The effectiveness decreased in the following order: 1) T3 50 micrograms/d (most effective), 2) (T4 50 micrograms/d + T3 12.5 micrograms) x 2, 3) T4 150 micrograms + iodide 150 micrograms/d, 4) T4 75 micrograms + T3 18.75 micrograms/d, 5) T4 200 micrograms/d, 6) T3 37.5 micrograms/d, 7) Iodide 300 micrograms/d, 8) T4 150 micrograms/d, 9) Iodide 150 micrograms/d (least effective) and 10) Placebo (not effective). The results show that T4 200 micrograms and T3 50 micrograms are roughly equipotent, and slightly more effective than 300 micrograms of Iodide. Taking into consideration the side effects (increase in pulse rate, shortening of the Achilles tendon reflex) did not change the order of effectiveness in an important way. The clinical outcome correlated in general with the suppression of the 131I uptake (r = 0.220, p = 0.03) and the TRH test (r = 0.248, p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗
PubMed1992

[Two cases of lateral approach for thoraco-lumbar junctional lesions: experiment of Kaneda's device].

Case 1: a 32-year-old woman was admitted to our hospital with major complaints of gait disturbance and urinary incontinence. The tendon reflex was markedly increased in the bilateral lower extremities, and both Babinski's reflex and clonus were strongly positive. Myelography revealed complete block in the 10th thoracic vertebral level. On April 15, 1989, a tumor in the vertebral region was exposed and excised via a right posterolateral approach. Kaneda's device was used for internal fixation. The tumor was diagnosed as myeloma histologically. The postoperative course was uneventful. Postoperatively, the patient became capable of walking by herself. Case 2: an 18-year-old woman was admitted because of burst fractures of the 1st and 2nd lumbar vertebrae due to a traffic accident in January of 1989. The fractured bones had been manually repositioned and fixed with plaster. However, the patient still had gait disturbance (intermittent claudication). Myelography revealed a complete block in the 2nd lumbar vertebral region. On May 7, the vertebral foramen was opened via a left anterolateral approach, and internal fixation was performed using Kaneda's device. Postoperatively, the patient recovered full ability to walk, and returned to normal social activity. From our experience, it is thought to be useful to employ a right posterolateral approach to the thoracic vertebrae, and a left anterolateral approach to the lumbar vertebrae. We used Kaneda's device for internal fixation, successfully. However, this device has the following disadvantages; (1) there are few plates designed for females, whose vertebrae are small, (2) it is difficult to preserve the arteries of Adamkiewicz and (3) postoperative MRI becomes impossible.

Adolescent↗
PubMed1991

Molecular analysis of the Smith-Magenis syndrome: a possible contiguous-gene syndrome associated with del(17)(p11.2).

We undertook clinical evaluation (32 cases) and molecular evaluation (31 cases) of unrelated patients affected with Smith-Magenis syndrome (SMS) associated with an interstitial deletion of band p11.2 of chromosome 17. Patients were evaluated both clinically and electrophysiologically for peripheral neuropathy, since markers showing close linkage to one form of Charcot-Marie-Tooth disease (CMT1A) map to this chromosomal region. The common clinical findings were broad flat midface with brachycephaly, broad nasal bridge, brachydactyly, speech delay, and hoarse, deep voice. Fifty-five percent of the patients showed clinical signs (e.g., decreased or absent deep tendon reflexes, pes planus or pes cavus, decreased sensitivity to pain, and decreased leg muscle mass) suggestive of peripheral neuropathy. However, unlike patients with CMT1A, these patients demonstrated normal nerve conduction velocities. Self-destructive behaviors, primarily onychotillomania and polyembolokoilamania, were observed in 67% of the patients, and significant symptoms of sleep disturbance were observed in 62%. The absence of REM sleep was demonstrated by polysomnography in two patients. Southern analysis indicated that most patients were deleted for five 17p11.2 markers--FG1 (D17S446), 1516 (D17S258), pYNM67-R5 (D17S29), pA10-41 (D17S71), and pS6.1-HB2 (D17S445)--thus defining a region which appears to be critical to SMS. The deletion was determined to be of paternal origin in nine patients and of maternal origin in six patients. The apparent random parental origin of deletion documented in 15 patients suggests that genomic imprinting does not play a role in the expression of the SMS clinical phenotype. Our findings suggest that SMS is likely a contiguous-gene deletion syndrome which comprises characteristic clinical features, developmental delay, clinical signs of peripheral neuropathy, abnormal sleep function, and specific behavioral anomalies.

Adolescent↗
PubMed1991

[A case of Behçet's disease associated with myopathy during cyclosporin treatment].

A 46-year-old male was admitted to the Department of Neurology complaining of gait disturbance. He was given a diagnosis of Behçet's disease and placed on colchicine (0.5-1.0 mg/day) for 7 months without improvement. Subsequently cyclosporin (290 mg/day) was added this regimen. However, 7 months after initiation of combined colchicine/cyclosporin therapy serum creatine kinase (CK) rose to 1,255 U/l. On admission, neurological examination revealed generalized muscle atrophy with predominant proximal muscle weakness and decreased deep tendon reflexes. No myalgia was noted. Laboratory tests demonstrated anemia, liver dysfunction, chronic renal failure and an elevated serum CK level. The plasma cyclosporin concentration was 220 ng/dl, which is within therapeutic limits. Motor unit potentials in electromyography of bilateral quadriceps muscles were generally of short duration and reduced amplitude. A biopsy of quadriceps muscle showed variability in the size of type 2 fibers and scattered small vacuoles. Some of the vacuoles resembled rimmed vacuoles. These vacuoles were stained positively for acid phosphatase. Electronmicroscopy revealed that these vacuoles contained dense bodies, myeloid bodies, and glycogen particles. Collectively suggesting that these structures are autophagic vacuoles. Cyclosporin was reduced to 200 mg/day with unchanged colchicine dose and bromocriptine, which potentiates cyclosporin effects, was started. Gradual recovery from muscle weakness ensued. These findings suggest that cyclosporin contributed to the pathogenesis of this myopathy. On increase in use of cyclosporin, one should consider the possibility of myopathy as one of its side effects especially in combination therapy with myotoxic drugs such as colchicine.

Behcet Syndrome↗
PubMed1991

[Guillain-Barré syndrome preceded by diarrhea with the infection of Campylobacter jejuni].

We report a 77-year-old woman with Guillain-Barré syndrome following Campylobacter jejuni infection. She was admitted complaining of mild weakness in the left leg. Seven days before, she had severe diarrhea, which continued several days. After admission, the weakness soon worsened resulting in tetraparesis, and the respiration became so impaired that she was supported by the artificial ventilator. Deep tendon reflexes were absent in four limbs, and no sensory disturbance was noted. CSF contained the protein as low as 20.4 mg/dl in concentration; no pleocytosis was seen. Muscle action potentials evoked by the stimulation of nerves were markedly reduced in amplitude, but conduction velocity along the nerve was decreased mildly. Campylobacter jejuni was detected by bacterial culture of the stool; the antibody was positively raised against this bacteria in serum. By 90 hospitals days, she was restored to spontaneous respiration.

Aged↗
PubMed1991

[A case of spinal epidural hematoma associated with idiopathic thrombocytopenic purpura].

Spinal epidural hematoma is a rare clinical entity, and the literature provides reports of 29 cases so far in Japan. A case of spinal epidural hematoma associated with idiopathic thrombocytopenic purpura diagnosed by CT scan and MRI is reported in detail with references to the literature. A 56-year-old female was admitted to our hospital on April 22, 1990, because of sudden onset of nuchal pain and right hemiparesis. Her consciousness was alert, but the deep tendon reflex was depressed, and pathological reflex such as Babinski's reflex was positive on the right side. Nuchal stiffness was observed. CT scan of the head revealed no abnormality, but the scan of cervical area showed an abnormal high density area in the right posterior region of the spinal cord at C2 - 3 level. MRI also revealed a low intensity area in the same region both in T1 and T2 weighted images. On admission, the platelet count was 10,000/microliters, and the bone marrow aspirate showed abundant megakaryocytes. The patient was diagnosed as having spinal epidural hematoma associated with idiopathic thrombocytopenic purpura. The patient was initially treated with a corticosteroid and a hyperosmotic agent. About 15 hours after the onset, her motor function began improving. Conservative therapy was continued, and she could walk 2 weeks after the onset. Spinal epidural hematoma is an uncommon disease commencing with back and radicular pain, paraplegia and rectovesical insufficiency. Early diagnosis and surgical decompression is generally imperative, although an exceptional remission without operation such as was observed in this case may occur.

Female↗
PubMed1991

[Juvenile-onset dystonia with bilateral atrophy of the basal ganglia on MRI].

A 40-year-old man was hospitalized for tremor of the right upper limb, gait disturbance and dysarthria. His course of development had been normal until the age of 14, when difficulties in speaking and walking, and tremor of the upper limb became evident following an episode of fever. His symptoms have been gradually worsening for the past 25 years. His elder sister showed similar clinical symptoms and progressive course of illness. The patient showed no indication of mental retardation. Neurological examination showed dysarthria, slow dyskinetic movement of the tongue, dystonic posture of the left hand, tremor of irregular frequency of the right upper limb, diminished tendon reflex, positive Romberg's sign, diminished vibratory and position sense in the lower limbs and pyramidal signs. Cystometry indicated defective voiding of the bladder. Magnetic resonance imaging of the brain showed bilateral atrophy of the putamina, globus pallidus, caudate nuclei and substantia nigra. MRI showed similar findings in her sister. By electrophysiological and pathological examination, disorders of other systems were evident, such as upper motor neurons, and sensory tract. GM1 and GM2 gangliosidosis appeared the most likely diagnosis, but were ruled out on the basis of the result of lysozomal enzyme assay and rectal biopsy. The present patient's condition may possibly be the result of an unknown metabolic disorder, or a new disease entity affecting various components of the nervous system.

Adult↗
PubMed1991

[Central motor conduction time in the pseudopolyneuritic form of amyotrophic lateral sclerosis].

Central motor conduction time (CMCT) from the cerebral motor cortex to the cervical segment of the spinal cord (C-CMCT) and CMCT from the cortex to the lumbar segment of the spinal cord (L-CMCT) were estimated using percutaneous electrical cortical, cervical and lumbar stimulation in 8 patients with pseudopolyneuritic form of amyotrophic lateral sclerosis (ALS). The results were compared to those in 18 patients with bulbar and common forms of ALS and 13 normal control subjects. Both the C-CMCT and the L-CMCT were remarkably prolonged in pseudopolyneuritic form of ALS as well as in bulbar and common forms of ALS. These results were consistent with the morphological findings that the large myelinated fibres in the corticospinal tract are depleted in pseudopolyneuritic form of ALS in which deep tendon reflexes are hypoactive and pyramidal sings are not obvious. The evaluation of CMCT is suggested to be useful for diagnosis of ALS in which upper motor neurone disorder is not manifested.

Adult↗
PubMed1991

[An autopsy case of Gerstmann-Sträusser-Scheinker's disease with spastic paraplegia as its principal feature].

A 38-year-old woman developed slowly progressive gait disturbance. At age 39 years she was admitted to our department because she could not walk without assistance. On neurological examination she was alert with normal mental functions. Horizontal nystagmus on both sides, minimal clumsiness in the left upper extremity on the finger-to-nose test and moderate degree of spasticity in bilateral lower extremities without evident motor weakness were present. The gait was spastic with small steps on a wide base. There was no sensory abnormalities. The deep tendon reflexes were hyperactive on both sides, on the lower extremities, with positive Babinski's sign. The sphincter functions were intact. During the following 5 years she gradually deteriorated and pseudobulbar palsy, emotional incontinence and the progressive dementia appeared in addition to severe spastic paraplegia. At age 45 years she was admitted to our nursing home and she died 3 months later, of pneumonia, on 6 years after the onset of her illness. Two elder sisters of her 7 siblings had the similar neurologic illness. The brain weighed 1,060 g. There was mild atrophy of cerebrum, cerebellum and brainstem. There were neuronal loss and gliosis in layers IV-VI of cerebral cortex with no evidence of the spongy state. Cerebellar cortex, cerebellar peduncles and spinocerebellar tracts were preserved. There was marked degeneration of corticospinal tract from cerebral peduncle to lateral funiculus of lumbar spinal cord. The most prominent feature was appearance of numerous multicentric amyloid plaques, which were marked in layers I-III of cerebral cortex and to a lesser extent in corpus striatum, hippocampus and the white matters of cerebrum and cerebellum.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyloid↗
PubMed1991

[The correlation of consciousness level and the concentration of CSF ammonia in a patient with adult-type citrullinemia].

A 29-year-old man who had a taste for peanuts frequently showed abnormal behaviors. Physical examination revealed consciousness disturbance associated with flapping tremor, hypotonus in the extremities, and hypoactive deep tendon reflexes. Laboratory examination showed hyperammonemia with mild liver injury. A level of serum citrulline was 14 times higher than the upper limit of normal. A diagnosis of type 2 citrullinemia (Seheki et al) was established by the decreased argininosuccinate synthetase (ASS) in liver with low amount of ASS protein and normal kinetic properties. Diurnal fluctuation of consciousness level in this patient was not correlated with the concentration of ammonia in serum, but with that in cerebrospinal fluid. Main metabolic pathway of ammonia in brain is considered to be localized in astrocytes which have receptors for glucocorticoids. Glucocorticoids induce additional glutamine synthetase activity. Circadian rhythm of cortisol level might play a role in diurnal fluctuation of consciousness level in patients with citrullinemia.

Adult↗
PubMed1991

[A case of HTLV-1 associated myelopathy and adult T-cell leukemia, presenting unique muscle pathology including rimmed vacuole].

A 63-year-old man developed muscular atrophy and weakness in his four extremities since 1983, and was pointed out to have smoldering ATL by elevated HTLV-1 antibody titers in the serum (x 2,500) and CSF (x 32) in 1985. Neurological examinations revealed proximal muscular weakness and atrophy of four extremities, and mild spasticity of both legs. Deep tendon reflexes were hypoactive in both arms and hyperactive in both lower extremities with ankle clonus and bilateral positive Babinski and Chaddock reflexes. These findings were compatible with HAM. His gait, however, was markedly waddling, requiring support. Muscle biopsy at left biceps muscle revealed inflammatory change with rimmed vacuoles, small group atrophy, and marked type 1 fiber predominance. These findings on muscle biopsy are different from those of previously reported cases with HAM, showing some similarities to inclusion body myositis or distal myopathy with rimmed vacuole.

Biopsy↗
PubMed1991

[Successful treatment of "steroid-immunosuppressant resistant" polymyositis with immunoadsorption].

We report a case of "steroid and immunosuppressant-resistant" polymyositis that was successfully treated with immunoadsorption. A 46-year-old man was admitted to Shinshu University Hospital on June 2, 1989, with the chief complaint of muscle weakness and pain. He had a 1.5-year history of frequent episodes of Raynaud's phenomenon. Five months before presentation, he noticed muscle weakness and pain in the proximal muscles of his extremities. One month after the onset of these symptoms, his body temperature increased to 38 degrees C and remained elevated until the following month. He subsequently entered a local hospital. He was found to have diminished strength in all limbs that was more marked in the proximal areas. The muscle weakness and pain progressed until the patient was no longer able to walk. Muscle biopsy of the left quadriceps femoris showed mononuclear cell infiltration in the endomyosium that was accompanied by phagocytosis and interstitial fibrosis. Based on these findings, a diagnosis of polymyositis was made. During hospitalization, the weakness continued to worsen despite pulse therapy with methylprednisolone 1000 mg per day for 3 days and the administration of prednisolone 100 mg and azathioprine 100 mg per day. The patient was transferred to our hospital for further evaluation and treatment. On physical examination, he demonstrated hair loss, soft palate aphthae, tonsillar injection, and cervical lymphadenopathy. Neurological examination revealed generalized weakness; the patient was barely able to move all of his limbs. All of the muscles in his extremities were swollen and hard, and he felt pain when they were grasped. Deep tendon reflexes were diffusely hypoactive.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigen-Antibody Complex↗
PubMed1991

[Supranuclear vertical gaze palsy and convergence nystagmus caused by unilateral riMLF lesion].

We report a case showing supranuclear vertical gaze palsy and convergence nystagmus caused by a unilateral lesion of the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). The patient was a 54-year-old female with mitral stenosis and regurgitation and atrial fibrillation, who suddenly developed vertigo and double vision. She was admitted to our hospital because of persisting diplopia 4 days after onset, although vertigo had resolved within 1 hour. On admission she was alert, but presented with supranuclear vertical gaze palsy and convergence nystagmus. Other cranial nerves were intact and motor strength, deep tendon reflexes, sensations were also normal. There were no cerebellar signs. Cranial MRI demonstrated a unilateral ischemic lesion at the left thalamo-mesencephalic junction that involved the unilateral riMLF. Cerebral angiography revealed no abnormalities. Vertical gaze palsy has been reported to be caused by a lesion involving bilateral riMLF or unilateral posterior commissure, and convergence nystagmus usually by a lesion near or within the dorsal mesencephalon. However, recent reports have demonstrated a histopathologic evidence that vertical gaze palsy was caused by unilateral riMLF lesion. The present case confirms clinically that both vertical gaze palsy and convergence nystagmus can be developed by a lesion of unilateral riMLF.

Brain Diseases↗
PubMed1991

[A case of spinal osteomyelitis detected by MRI].

A 75-year-old man was admitted because of chest pain and gait disturbance. He noticed pain in the left anterior chest regardless of exercise 3 months prior to admission. Two months later, the chest became smart with motion, followed by sensory disturbance of the lower extremities. On admission, he was anemic. His lower extremities showed exaggerated deep tendon reflexes with positive Babinski signs and an impairment of superficial and deep sense with sensory ataxia. Muscular weakness, muscular wasting, or urinary disturbance was not found. An X-ray film of his thoracic spine disclosed compression fracture and protein content of his cerebrospinal fluid was increased. Magnetic resonance image (MRI) of the ill spines revealed fusion of the bodies of the fifth and sixth thoracic vertebrae with a low signal intensity on T1-weighted images and a partially high signal intensity on T2-weighted images. The intervertebral disc was destroyed. Although histological or bacteriological confirmation was absent, characteristic MRI findings were compatible with spinal osteomyelitis. After antibacterial chemotherapy, his clinical symptoms improved and he came to be able to walk again.

Aged↗
PubMed1991

[Post-poliomyelitis late progressive muscular atrophy (PPMA)--clinical analyses of Japanese cases].

Clinical and epidemiologic analyses of PPMA in Japan based on the nation-wide case survey were reported, and differences between PPMA and ALS were discussed. The present survey covering the years from 1984 through 1991 cited 42 PPMA cases (30 male:12 female). The absolute incidence of PPMA is estimated 0.12/10(5) of the Japanese population (about 150 cases in total), which indicates 0.5% of the polio survivors. In Japan an actual increase of patients is noticed in these 10 years, which reflects the big epidemic of polio around 1950-60. The antecedent poliomyelitis occurred at the mean age of 2.6, mostly between 1940 and 1960. Residual paralysis was generally absent or only minimal. Late muscular atrophy and weakness were noticed at age from 16 to 63 y (mean:41.5), with the mean latency of 40.1 years after polio. Both polio-affected and unaffected site of the limb were equally involved by PPMA, but the left leg tends to be predominantly involved. Neurological symptoms were summarized as an asymmetrical proximal muscular atrophy and flaccid motor paresis in one or two limbs with decreased tendon reflexes. Fasciculation in 45.2%, myalgia in 28.6%, and hypesthesia in 28.5% were noticed. Electromyography and muscle CT scan showed marked selective neurogenic changes. In most cases symptoms are stable or slowly progressive, with some recovery by rest or rehabilitation and deterioration by over work and/or trauma. On regarding these clinical features, PPMA is essentially different from classical ALS. Long-term hyperfunction of survived neurons with potential fragility by polio infection is suspected to mediate PPMA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Nephrotic syndrome complicated with cerebral infarction: report of one case].

A 13-year-old boy was admitted to this hospital for evaluation of pitting edema of both legs. Three years ago, he had been diagnosed to have nephrotic syndrome. Two and half years ago, because of persistent heavy proteinuria, poor response to steroids and frequent relapse of disease, a renal biopsy was done; characteristics of IgM nephropathy was shown. About a year previously, the patient felt dizziness and weakness of the left side of his body upon awakening one morning. Neurologic examination showed loss of muscle tone, muscle power and deep tendon reflexes. Sensory and cranial nerve function were intact. Blood pressure was normal. The CT scan of brain showed a patch of low attenuation area in the right temporal region, obliteration of the right cortical sulci and mild compression of right lateral ventricle. A diagnosis of nephrotic syndrome with right cerebral infarction was made. The patient's condition became stable two days later after mannitol infusion, correction of electrolytes, and supportive therapy. According to literature, most cases of nephrotic syndrome complicate with renal thrombosis, pulmonary emboli, and deep vein thrombosis. Few cases complicate with cerebral thrombosis and infarction. If patient have low plasma albumin and anti-thrombin III level, hyperfunction of platelet aggregability and use long-term diuretic therapy, they may be at higher risk of thromboembolic complications. If thromboembolic complications exist, anticoagulation treatment should be instituted. Prophylactic therapy with aspirin or dicumarol is not currently recommended.

Adolescent↗
PubMed1991

Echocardiographic and pulsed Doppler features in glycogen storage disease type II of the heart (Pompe's disease).

Two cases of cardiac glycogen storage disease type II are described: the first one, male aged 3 months, presented with generalized muscular hypotonia and decreased deep tendon reflexes; a 2/6 systolic murmur was audible at the left sternal border; chest X-ray and ECG were consistent with left ventricular hypertrophy; an echocardiogram disclosed an impressive and diffuse cardiac hypertrophy; the pump function appeared preserved and the estimated ejection fraction was about 70%. Pulsed wave Doppler demonstrated a normal envelope of mitral flow with E/A ratio = 1.27 in averaged 20 beats. The patient died suddenly at 6 months of age. The second patient was a female 4 months old with generalized muscular hypotonia. ECG and chest X-ray were consistent with left ventricular hypertrophy; 2D echocardiogram showed diffuse hypertrophy with estimated ejection fraction of 68% and an almost normal aspect of the mitral flow curve, with E/A ratio of 1.18. This child died at 13 months of age of cardiopulmonary insufficiency. In both cases the diagnosis was made by muscular biopsy and biochemical tests (alpha 1-4 glucosidase deficiency). We stress the fact that, despite the severe and diffuse hypertrophy, the pump function and the ventricular filling did not seem compromised.

Cardiomegaly↗