Dengue Myopathy Detected by Whole-Body Muscle STIR MRI

Sir, India reported around 180,000 cases of dengue in 2017.[1,2] Dengue associated neurological (DAN) complications include myalgias, myopathy, hypokalemic paralysis, rhabdomyolysis, Guillain-Barre syndrome, anterior horn cell involvement, peripheral neuropathies, plexopathies, or/and mononeuritis multiplex.[3] Brain MRI occasionally shows diffuse involvement of grey and white matter, micro or macrohemorrhages and PRES syndrome in ~50% of DAN. Dengue myopathy (DeM) is characterized by an acute symmetric proximal hyporeflexic self-resolving weakness.[4,5] Muscle MRI has not yet been reported in dengue. A 56-year-old man presented with altered mental status, seizures, fever, and severe myalgia for 3 days. CSF studies and MRI brain were normal. Dengue NS1 (day 2) and dengue IgM (day 7) were positive. CPK levels were 96,000 U/L. Serum electrolytes and renal functions were normal. On day 10, a whole-body STIR MRI showed diffuse muscle STIR hyperintensities in the pelvic, thigh, and shoulder girdle muscles (on left more than on right) [Figure 1]. He was treated symptomatically and discharged without sequelae on day 15.Figure 1: Coronal STIR whole-body MRI sequence showing hyperintensities in lower limb muscles and shoulder girdle muscles asymmetrically. Mild bilateral pleural effusions and mild ascites are also seenA 43-year-old woman was admitted with severe headache, fever, and myalgia of 4 days duration. CSF showed 270 cells with 85% neutrophils, normal protein, and sugar levels. On day 2, dengue IgM was positive. Serum CPK level was 70 U/L and electrolytes were normal. On day 17, she had persistent myalgia and frequent knee buckling. Serum CPK was 650 U/L. She had diffuse muscle tenderness and proximal upper and lower limb weakness [MRC grade 4/5] with hyporeflexia. EMG showed small polyphasic potentials [compatible with a myopathic process] with scattered fibrillations and positive sharp waves. On day 18, whole-body muscle MRI showed asymmetric STIR muscle hyperintensities in the pelvic muscles and lower limbs [Figure 2]. A right quadriceps muscle biopsy showed nonspecific changes. After symptomatic treatment, her condition improved within 2 months.Figure 2: Coronal STIR whole-body MRI sequence showing asymmetrical right more than left lower limb muscle hyperintensities (gluteal, quadriceps, hamstring and calf muscles)A 53-year-old woman presented with a 5-day history of headache, fever, and myalgia. Examination revealed fever, a distal extremity maculopapular rash, and diffuse muscle tenderness. Dengue NS1 was positive [day 1]. CSF showed 25 lymphocytes, with normal protein and sugar. On day 7, her dengue IgM was positive. On day 10, severe proximal muscle weakness, hyporeflexia, and diffuse muscle tenderness were noted. Serum CPK levels were 1500 U/L. Serum electrolytes were normal. EMG showed only small myopathic potentials. On day 16, whole-body muscle STIR MRI imaging showed asymmetrical muscle hyperintensities involving the lower limbs more than the upper limbs. Diffuse subcutaneous hyperintensities were also noted [Figure 3]. She improved gradually and was asymptomatic at a 3-month follow-up visit.Figure 3: Coronal STIR whole-body MRI sequence showing asymmetrical muscle hyperintensities involving predominantly lower limbs. Subcutaneous fluid and bilateral pleural effusions are also seenMyalgia is seen in more than 90% of patients with dengue while DeM is less common.[6,7] DeM presents with mild pure motor weakness, an acute symmetric proximal hyporeflexic weakness, quadriplegia, bulbar weakness, respiratory insufficiency, hypokalemic weakness, fulminant rhabdomyolysis, or Guillain-Barre syndrome.[8,9] More than 90% of patients recover spontaneously within 4–6 weeks. EMG usually shows myopathic potentials with denervation changes.[4] DeM is postulated to be caused by direct viral muscle invasion in the viremic stage. Intracellular calcium accumulates in muscles activating mitochondrial-dependent apoptotic cell death pathways and thereby myonecrosis.[10] Infection also stimulates the release of serum tumor necrosis factor-α [TNF-α], cytotoxins and IL-6, 13, and 18 which increase the vascular permeability and lead to shock, aggravating myocyte injury. MRI muscle imaging shows two patterns in myopathies; in acute cases, muscle shows an inflammatory/edema pattern or a mass lesion [Pattern 1] while in chronic cases, muscle atrophy or fatty infiltration is seen [Pattern 2].[11] In pattern 1, MRI shows high signal intensities on STIR imaging and T2-weighted imaging, with low to intermediate signal on T1-weighted imaging. In pattern 2, muscles undergo atrophy followed by fatty infiltration. Our cases showed pattern 1 as the MRI was performed in the acute phase of the illness (an average of 2 weeks from the onset of illness). DeM involved the lower limb muscles more than the upper limbs and muscle involvement was patchy and asymmetric. In the literature, a muscle biopsy is abnormal in less than 20% of cases of DeM. Hence, most cases are diagnosed with a combination of clinical presentation and EMG. As our cases demonstrate, whole-body MRI muscle imaging can easily demonstrate DeM.[3] In conclusion, whole-body muscle MRI can assist in the early detection of DeM or pickup subclinical DeM. It can obviate the need for invasive muscle biopsies and complements EMG studies. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.