Myasthenia gravis can cause camptocormia: Figure 1

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Abstract
In February 2009, a 75-year-old woman with a history of hypertension and angina noticed lower extremity weakness, numbness below the trunk and forward flexion of the lumbar spine. In April, she underwent surgery to treat ossified thoracic yellow ligaments, and the numbness resolved. However, weakness and forward flexion of the lumbar spine gradually worsened, and in August she required a cane to walk. In October, she presented with dropped head. The severity of forward flexion of the lumbar spine and dropped head increased in parallel to general weakness when she continued to walk. Assistance in daily living was eventually required. In April 2010, ptosis developed, and in August she noticed respiratory difficulty during routine activities, leading to admission to our hospital. Bilateral ptosis, restricted upward eye movements and muscle weakness in all four limbs and the neck were evident. She demonstrated abnormal posture of the trunk, with marked flexion of the thoracolumbar spine and dropped head on natural standing (figure 1A,C). She could not straighten her back with maximal effort (figure 1D), and she had to raise her chin with her hand to look forwards. Abnormal posture increased while walking and abated in the recumbent position. Mildly increased deep tendon reflexes with no pathological reflex and mild sensory impairment in the lower limbs were also evident, which seemed to cause preoperative spinal disorder. The quantitative MG score2 was 26. The levels of serum creatine kinase (54 U/l), pyruvic acid (0.6 mg/dl) and lactate dehydrogenase (6.8 IU/l) were not abnormally elevated. The antiacetylcholine binding receptor antibody titre was 150 nmol/l (normal upper limit, >0.2 nmol/l). After injecting edrophonium, the abnormal postures resolved, and the severities of ptosis, oculomotor disorder and general weakness decreased (figure 1A,B). Repeated stimulation studies demonstrated a decremental response at a slow stimulation rate in the orbicular muscle of the eye and the abductor digiti minimi. A CT scan of the chest showed evidence suggesting a mediastinal thymoma. Oxygen and carbon dioxide pressures on arterial blood gas analysis were 74.1 and 45.2 mm Hg, respectively. Electromyography of the paraspinal muscles at the levels of C7, T4, Th8 and Th12 and the sternocleidomastoideus showed no evidence of myopathic motor unit action potentials. Other muscles (biceps, triceps, adductor of thumb, quadriceps, gastrocnemius and tibialis anterior) were also apparently not affected. MRI scanning from the C1 to L5 vertebrae showed mild atrophy in the erector muscles, but no abnormal signals of these muscles or compression of the spinal cord was evident. Oral prednisolone was gradually increased to 25 mg/day, and the severity of disease decreased. In February 2011, the quantitative MG score and antiacetylcholine binding receptor antibody titre had decreased to 18 and 34, respectively. The patient could walk unaided and did not require oxygen. The abnormal postures markedly improved (figure 1E), and the patient could avert her back with maximal effort (figure 1F). An abnormal posture no longer occurred while walking. She received a thymectomy in April, and a diagnosis of thymoma was confirmed histologically.

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