Hamstring Muscle Cramp Visualized on Bone Single-Photon Emission Computed Tomography/Computed Tomography Hybrid Imaging.

ABSTRACT: It is well recognized that bone-seeking radiotracers localize in muscles sustaining an injury from various causes (e.g., strenuous physical activity, trauma, hereditary myopathies, inflammatory myositides, medications, electrical burns, etc.). This report presents the case of an active 50-yr-old man (body mass index = 29) that was recently referred to our nuclear medicine department for bone scintigraphy, for the skeletal staging of a newly diagnosed prostate adenocarcinoma. The scan findings were unremarkable for its oncological indication but revealed extraosseous radiotracer absorption in the medial region of the hamstrings bilaterally. Hybrid scintitomography (single-photon emission computed tomography) with computed tomography indicated that this uptake involved the semitendinosus muscle. On a more meticulous repeat history questioning, he recalled experiencing muscle cramps on both posterior thighs 5 days earlier, during intense work-related physical activity (plumbing) under warm environmental conditions. The combination of strenuous exercise with likely dehydration contributed to bilateral self-limiting heat cramps of the hamstrings, leading to an inconsequential localized minor rhabdomyolysis that was discovered coincidentally a few days later during a bone scan. Although extraskeletal absorption of bone-seeking radiotracers in muscles is widely documented as a result of exertion or injury, this is the first report of radiotracer absorption induced by cramping.

Cine MRI during spontaneous cramps in women with menstrual pain.

BACKGROUND: The lack of noninvasive methods to study dysmenorrhea has resulted in poor understanding of the mechanisms underlying pain, insufficient diagnostic tests, and limited treatment options. To address this knowledge gap, we have developed a magnetic resonance imaging-based strategy for continuously monitoring the uterus in relationship to participants' spontaneous pain perception. OBJECTIVE: The study objective was to evaluate whether magnetic resonance imaging can detect real-time changes in myometrial activity during cramping episodes in women with dysmenorrhea, with a handheld squeeze bulb for pain reporting. STUDY DESIGN: Sixteen women with dysmenorrhea and 10 healthy control women both on and off their menses were evaluated with magnetic resonance imaging while not taking analgesic medication. Continuous magnetic resonance imaging was acquired using half-Fourier acquisition single-shot turbo spin echo sequence along with simultaneous reporting of pain severity with a squeeze bulb. Pearson's coefficient was used to compare results between reviewers. Proportional differences between women with dysmenorrhea and controls on/off menses were evaluated with a Fisher exact test. The temporal relationships between signal changes were evaluated with Monte Carlo simulations. RESULTS: Spontaneous progressive decreases in myometrial signal intensity were more frequently observed in women on their menses than in the absence of pain in the same women off their menses or participants without dysmenorrhea (P < .01). Women without reductions in myometrial signal intensity on their menses either had a history of endometriosis or were not in pain. Observations of myometrial events were consistently reported between 2 raters blinded to menstrual pain or day status (r = 0.97, P < .001). Episodes of cramping occurred either immediately before or 32-70 seconds after myometrial signal change onset (P < .05). CONCLUSION: Transient decreases in myometrial uterine T2-weighted signal intensity can be reliably measured in women with menstrual pain. The directionality of signal change and temporal relationship to pain onset suggest that cramping pain may be caused by a combination of uterine pressure and hemodynamic dysfunction.

Cerebrovascular disease related to COL4A1 mutations in HANAC syndrome.

BACKGROUND: COL4A1 mutations cause familial porencephaly, infantile hemiplegia, cerebral small vessel disease (CSVD), and hemorrhagic stroke. We recently described hereditary angiopathy with nephropathy, aneurysm, and muscle cramps (HANAC) syndrome in 3 families with closely localized COL4A1 mutations. The aim of this study was to describe the cerebrovascular phenotype of HANAC. METHODS: Detailed clinical data were collected in 14 affected subjects from the 3 families. MRI and magnetic resonance angiography (MRA) were performed in 9 of them. Skin biopsies were analyzed by electron microscopy in affected subjects in the 3 families. RESULTS: Only 2 of 14 subjects had clinical cerebrovascular symptoms: a minor ischemic stroke at age 47 years and a small posttraumatic hemorrhage under anticoagulants at age 48 years. MRI-MRA showed cerebrovascular lesions in 8 of 9 studied subjects (mean age 39.4 years, 21-57 years), asymptomatic in 6 of them. Unique or multiple intracranial aneurysms, all on the carotid siphon, were observed in 5 patients. Seven patients had a CSVD characterized by white matter changes (7/7) affecting subcortical, periventricular, or pontine regions, dilated perivascular spaces (5/7), and lacunar infarcts (4/7). Infantile hemiplegia, major stroke, and porencephaly were not observed. Skin biopsies showed alterations of basement membranes at the dermoepidermal junction associated with expansion of extracellular matrix between smooth vascular cells in the arteriolar wall. CONCLUSION: The cerebrovascular phenotype in hereditary angiopathy with nephropathy, aneurysm, and muscle cramps syndrome associates a cerebral small vessel disease and a large vessel disease with aneurysms of the carotid siphon. It is consistent with a lower susceptibility to hemorrhagic stroke than in familial porencephaly, suggesting an important clinical heterogeneity in the phenotypic expression of disorders related to COL4A1 mutations.

[Popliteal vein entrapment in patients with unspecific symptoms of venous insufficiency]. / Belastungs- oder lageabhängige Schwellung der Wadenmuskulatur mit Spannungsgefühl und krampfartigen Schmerzen.

Popliteal vein entrapment must be taken in consideration in patients with symptoms of venous insufficiency. Leg edema, swelling, calf pain, and muscle cramps are all unspecific signs. Most patients thus far have presented with deep vein thrombosis or chronic venous insufficiency. Popliteal entrapment syndrome must be taken into account in younger patients in whom predisposing factors are absent and chronic calf swelling is notable. Diagnosis is easily confirmed by noninvasive stress testing with duplex imaging and pencil Doppler probe placed over the posterior tibial artery. Additionally, digital subtraction angiography with the foot in neutral and dorsi plantarflexion is recommended for arterial entrapment. Surgery is advisable for treatment and can be done without significant morbidity. In asymptomatic patients, we suggest using the term "popliteal vein entrapment phenomenon." We describe different etiologies of popliteal vein entrapment in three cases and present a review of the literature.

Deficient activation of the motor cortical network in patients with writer's cramp.

OBJECTIVE: To study regional cerebral blood flow (rCBF) in patients with simple writer's cramp using PET to identify regions that malfunction. BACKGROUND: Several lines of evidence indicate impaired cortical function in patients with focal dystonia, but the precise pathophysiology is still unknown. METHODS: Seven patients with writer's cramp were compared with seven age- and sex-matched control subjects. Control subjects and patients were scanned during sustained contraction, tapping, and writing with the right hand. After realignment and stereotactic normalization of the scans, all tasks were compared with a rest condition. For each task, an intra- and intergroup comparison was performed using statistical parametric mapping. For each condition and within groups, rCBF correlation analysis was performed between some selected regions that were activated during movement. RESULTS: In control subjects and patients, significant increases of rCBF were observed for each task in areas already known to be activated in motor paradigms. The intergroup comparison disclosed less activation in writer's cramp patients for several areas for all three tasks. This decrease reached significance for the sensorimotor cortex during the sustained contraction task and for the premotor cortex during writing. rCBF correlation analysis showed different patterns between control subjects and patients. At rest and during writing, the correlations between the putamen and premotor cortical regions and between the premotor cortical regions themselves were stronger in control subjects. CONCLUSIONS: Deficient activation of premotor cortex and decreased correlation between premotor cortical regions and putamen suggest a dysfunction of the premotor cortical network in patients with writer's cramp possibly arising in the basal ganglia. The dysfunction is compatible with a loss of inhibition during the generation of motor commands, which in turn could be responsible for the dystonic movements.

Cerebral and cerebellar activation in correlation to the action-induced dystonia in writer's cramp.

The pattern of brain perfusion of four patients with writer's cramp and four control subjects were examined using positron emission tomography scans after [(15)O] butanol injections. Each subject was scanned 12 times to cover three repetitions of four different motor tasks with the right hand. Drawing of horizontal lines and variable durations of the writing of a prelearned text were performed in a pseudorandom order, the latter task commencing either simultaneously with or 30 sec or 120 sec before the tracer injection. The perceived difficulty and signs of dystonia progressed in correlation to the duration of writing. Statistical parametric maps were calculated to test hypotheses of regional specific effects dependent on the performed motor tasks. The patients with writer's cramp had progressively increased activity in the left primary sensorimotor and premotor cortices, the left thalamus, and the cerebellum with a right-side predominance in correlation to the duration of writing. The regions with activity increases thus corresponded to a cerebrocerebellar motor circuit. The duration of writing correlated to a progressive reduction of activity in the patients' left supramarginal and angular gyri (Brodmann areas 40 and 39) and an inferior part of the left temporal lobe (area 20). The control subjects had neither a significant increase or decrease of activity in correlation to the duration of writing. Group-specific differences were confirmed statistically in split-plot interaction analyses.

Abnormal cortical responses in patients with writer's cramp.

We evaluated sensorimotor processing in patients with writer's cramp using PET and H2(15)O blood flow scans. The study included six right-handed patients with unilateral writer's cramp and eight right-handed normals. Subjects had blood flow scans at rest and during vibration of either the "affected" or "unaffected" hand. Vibration produced a consistent peak response in primary sensorimotor area (PSA) and supplementary motor area (SMA), both contralateral to the vibrated hand. Both responses were significantly reduced approximately 25% in patients with writer's cramp (PSA, p = 0.002; SMA, p = 0.02) whether vibrating the affected or unaffected hand. This indicates that patients with unilateral writer's cramp have bilateral brain dysfunction. These data provide objective evidence of abnormal central sensorimotor processing in writer's cramp.

Computed tomographic findings in manifesting carriers of Duchenne muscular dystrophy.

Clinical and computed tomographic (CT) findings in 3 manifesting carriers of Duchenne muscular dystrophy are reported. CT proved to be an important adjunct to the clinical examination: in all our 3 cases a decrease in density was found in various non-paretic muscles.