APIK Journal of Internal Medicine

: 2022  |  Volume : 10  |  Issue : 2  |  Page : 131--132

Basedow's paraplegia, a rare presentation of severe untreated hyperthyroidism

Saqlain Mohamed, Jayachandra, Nagaraj Nanjundaiah 
 Department of General Medicine, Sapthagiri Institute of Medical Sciences and Research Centre, Bengaluru, Karnataka, India

Correspondence Address:
Dr. Saqlain Mohamed
Department of General Medicine, Sapthagiri Institute of Medical Sceinces and Research Centre, Bengaluru, Karnataka


Typical presentations of hyperthyroidism are palpitation, nervousness, tremor, malaise, and weight loss. Hyperthyroidism affects nearly every system in the body, and some patients may manifest neurologic symptoms. Atypical presentations of hyperthyroidism often pose a great challenge in diagnosis and treatment. We report a case of Basedow's paraplegia, A 45-year-old male auto driver by occupation presented with complaints of weight loss of 15 kg in 2 months and weakness of the lower extremities for 1 month. On examination, he had weakness of both lower limbs and on investigation, he was found to be in severe hyperthyroid status, other investigations done to look for the causes of weakness of lower limbs were negative. The patient was treated for hyperthyroidism and gradual improvement of the weakness was observed.

How to cite this article:
Mohamed S, Jayachandra, Nanjundaiah N. Basedow's paraplegia, a rare presentation of severe untreated hyperthyroidism.APIK J Int Med 2022;10:131-132

How to cite this URL:
Mohamed S, Jayachandra, Nanjundaiah N. Basedow's paraplegia, a rare presentation of severe untreated hyperthyroidism. APIK J Int Med [serial online] 2022 [cited 2022 Jul 1 ];10:131-132
Available from: https://www.ajim.in/text.asp?2022/10/2/131/338147

Full Text


Lower limb weakness related to thyroid disorder was first noted by Charcot in 1889 and Joffrey called it Basedow's paraplegia in 1894.[1] The classical symptoms of Basedow's paraplegia are the subacute symmetric weakness of lower extremities with areflexia, without sensory or sphincter involvement.[1] Though the neuromuscular and primary muscle disorders in association with hyperthyroidism are well recognized, hyperthyroid neuropathy is uncommon.[2] Duyff et al. concluded at the end of their studies that muscle weakness in hyperthyroidism may be due to a functional muscle weakness rather than a myopathy. They also demonstrated a statistically significant correlation between the level of mean FT4 concentrations and the presence of paresis[3] This atypical presentation may lead to delay in the treatment of hyperthyroidism.

 Case History

A 45-year-old male autodriver by occupation presented with weight loss of 15-kg in 2 months and weakness of the lower extremities from 1 month. He denied the use of drugs, alcohol, or tobacco and had no recent history of trauma. On arrival, his vital signs were within normal limits with the exception of the heart rate, which was 104 beats/min. Rest of the physical examination was unremarkable. The neurologic examination revealed symmetric paraparesis (muscle strength 2/5) with areflexia. Fasciculations, myoclonus, and muscle atrophy were absent. The cranial nerves and sensation were intact. The laboratory tests concluded: Complete blood counts, electrolytes, glucose, calcium, phosphates, liver, renal function tests, and creatine phosphokinase were normal. Urine was negative for porphobilinogens. Blood, urine, and stool cultures were negative. Campylobacter was not detected in stool. There was no albumino cytological dissociation in the cerebrospinal fluid and other parameters were within the normal limits. Magnetic resonance imaging of the brain and spine was normal lesion. Nerve conduction study demonstrated the slowing of motor and sensory nerve velocity conductions, which was compatible with polyneuropathy. Electromyography showed fibrillations, positive sharp waves, and occasional fasciculation in right abductor pollicis brevis, quadriceps femoris, tibials anterior and extensor digitorum brevis. Motor unit potentials were large in amplitude, significant polyphasic potentials were seen and recruitment was incomplete. The Tensilon test was negative. Thyroid-stimulating hormone was <0.015 (normal 0.3–4.5), serum total thyroxine (T4) was 20.0 mcg/dl (normal 5.05–12.43 mcg/dl), total triiodothyronine (T3) was 2.48 ng/ml (normal 0.67–1.62 ng/ml), and free t4 levels were 40.77 ng (normal 6.4–20.6 ng). Technetium scanning revealed the hyperfunctioning state of the thyroid gland [Figure 1]. Methimazole 20 mg daily and propranolol of 160 mg daily were administered to control the hyperthyroid state. The paraplegia improved gradually during his hospital stay but incompletely. One month after the initiation of antithyroid treatment, the patient could walk with the assistance of a walker (muscle strength 4/5).{Figure 1}


Classical manifestations of hyperthyroidism were absent in this patient with the exception of his weight loss. Instead, in this case, hyperthyroidism presented with weakness of the lower limbs, a condition referred to as Basedow's paraplegia.[3] Hyperthyroidism may be associated or present with variety of neuromuscular disorders, including thyrotoxic myopathy, exophthalmic ophthalmoplegia, periodic paralysis, and myasthenia gravis. In contrast to muscle, peripheral nerve involvement in severe hyperthyroidism is very rare and has recieved little attention. This acute peripheral neuropathy is characterized by both proximal and distal leg weakness, decreased tendon reflexes, minimal or no sensory disturbance, and the absence of sphincter involvement.[4] An electrophysiologic study has shown mixed axonal and demyelinating sensorimotor neuropathy.[5] Although rare, peripheral neuropathy may be an initial clinical feature of hyperthyroidism.[5] The unique clinical features and exclusion of other neuromuscular diseases facilitated the diagnosis of Basedow's paraplegia. The manner in which thyroid abnormalities mediate neurologic dysfunction is unclear. Prompt treatment of hyperthyroidism results in gradual remission of paraplegia. Nevertheless, recovery of the weakness of the lower limbs may be incomplete even if the patient is restored to an euthyroid state.


We conclude by mentioning that physicians should consider hyperthyroidism as a differential diagnosis in a patient presenting with, bilateral lower limb weakness, and prompt treatment should be started while looking for other causes.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published, and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Feibel JH, Campa JF. Thyrotoxic neuropathy (Basedow's paraplegia). J Neurol Neurosurg Psychiatry 1976;39:491-7.
2Pandit L, Shankar SK, Gayathri N, Pandit A. Acute thyrotoxic neuropathy – Basedow's paraplegia revisited. J Neurol Sci 1998;155:211-4.
3Ali A, Malik WT, Raja U, Khan FA, Javaid I. Thyroid storm, a Mimicker of Guillain-Barre syndrome: A case report. Cureus 2020;12:e9918.
4Chen YH, Lin HJ, Chen KT. Rare presentations of hyperthyroidism – Basedow's paraplegia and pancytopenia. Am J Emerg Med 2009;27:258.e1-2.
5Smith L, Kemp T, van der Meyden CH, Schutte CM. Case report: Basedow paraplegia: A possible misnomer. South Afr Med J 2015;105:875.