Reversible isolated sensory axonal neuropathy due to cobalamin deficiency

Torre, Chiara Dalla; Lucchetta, Marta; Cacciavillani, Mario; Campagnolo, Marta; Manara, Renzo; Briani, Chiara

doi:10.1002/mus.22319

Cited by 15 publications

(7 citation statements)

References 18 publications

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“…Nevertheless, our patient did not notice any visual limitations. In addition to the lesion in the cervical myelon, electroneurography revealed the existence of an axonal sensorimotor polyneuropathy, which is also common for a lack of cobalamin [33]. As expected in this context, liquor analysis did not reveal an infectious or chronic inflammatory process.…”

Section: Discussionmentioning

confidence: 73%

Rapid healing of a patient with dramatic subacute combined degeneration of spinal cord: a case report

Roessler

Wolff

2017

BMC Res Notes

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BackgroundPrevalence of cobalamin deficiency is high especially in older patients and an immediate therapy start is necessary to prevent irreversible neurological damages. Unfortunately, the diagnosis of cobalamin deficiency is difficult and at present, there is no consensus for diagnosis of this deficiency. Therefore, we aim to elucidate a meaningful diagnostic pathway by a case report with an initially misleading medical history.Case presentationA 57 year-old Caucasian man suffering from dramatic myelosis of the cervical posterior columns. Apart from associated neurological symptoms (tactile hypaesthesia, reduced vibration sensation, loss of stereognosis and of two-point-discrimination) there were no further complaints; especially no gastrointestinal, haematological or psychiatric disorders were provable. Cobalamin (vitamin B12) serum level was normal. The diagnosis of subacute combined degeneration of spinal cord was confirmed by an elevated methylmalonic acid, and hyperhomocysteinemia. Cobalamin deficiency was caused by asymptomatic chronic atrophic inflammation of the stomach with a lack of intrinsic factor producing gland cells. This was revealed by increased gastrin and parietal cell antibodies and finally confirmed by gastroscopy. Parenteral substitution of cobalamin rapidly initiated regeneration.ConclusionsThis case demonstrates that normal cobalamin serum levels do not rule out a cobalamin deficiency. In contrast, path-breaking results can be achieved by determining homocysteine, holotranscobalamin, and methylmalonic acid.

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Section: Discussionmentioning

confidence: 73%

Rapid healing of a patient with dramatic subacute combined degeneration of spinal cord: a case report

Roessler

Wolff

2017

BMC Res Notes

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“…8 As mentioned previously, nutritional deficiencies can cause significant neuropathies as well. 1,2,3,4,5,6 Often times, these neuropathies tend to be axonal, but can have demyelinating features as well. 5 These malnutritionrelated neuropathies can also be complicated by comorbid alcoholism which makes diagnosing a singular cause of the neuropathy difficult.…”

Section: Discussionmentioning

confidence: 99%

“…1 There are numerous vitamins and minerals whose deficiencies have been found to cause profound neuropathies including thiamine, cobalamin, pyridoxine, vitamin E, and copper to name a few. 1,2,3,4,5,6 A singular nutritional cause is often difficult to determine as some patients may have coexisting alcoholism.…”

Section: Introductionmentioning

confidence: 99%

A Case of Significant Malnutrition Presenting as Acute Sensorimotor Axonal Neuropathy

Arnone¹,

Sultan²

2017

WVMJ

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Nutritional status is an important, but often overlooked, component of care for patients being seen in any number of subspecialty clinics. The neurologic ramifications of nutritional deficiencies tend to present in the later stages of prolonged malnutrition. A 34 year-old woman with a history of alcoholism presented to the emergency department with two weeks of worsening gait imbalance, diffuse paresthesia, allodynia, and weakness of all extremities. The physical examination yielded diffuse loss of sensation to all sensory modalities in a length-dependent manner and complete lack of deep tendon reflexes in all extremities. There was also mild 4/5 weakness of proximal musculature of upper and lower extremities. Nerve conduction studies showed a diffuse sensorimotor axonal neuropathy that was worse in the lower extremities compared to the upper extremities. Laboratory evaluation yielded significant deficiencies that included calcium, pyridoxine, vitamin E, folate, borderline low thiamine, and elevated homocysteine levels. This was a unique case of severe malnutrition manifesting as an acute diffuse axonal neuropathy. Lower socioeconomic status with concurrent alcohol use can lead to a bevy of neurologic conditions as seen in our patient.

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“…The B 12 deficient peripheral neuropathy is mainly sensory and of axonal pathology [ 17 ]. Early diagnosis is critical because neuropathies due to folate and cobalamin deficiencies are potentially reversible [ 17 , 18 ]. In adults, total body cobalamin content is 2–5 mg. A complete discontinuation in cobalamin absorption will take 3–5 years to deplete cobalamin stores [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Myanmarese Neuropathy: Clinical Description of Acute Peripheral Neuropathy Detected among Myanmarese Refugees in Malaysia

Hiew

Santhi

Shanthi

et al. 2014

International Scholarly Research Notices

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Background. Since 2008, we have observed an increasing number of Myanmarese refugees in Malaysia being admitted for acute/subacute onset peripheral neuropathy. Most of them had a preceding history of starvation. Methods. We retrospectively studied the clinical features of all Myanmarese patients admitted with peripheral neuropathy from September 2008 to January 2014. Results. A total of 24 patients from the Chin, Rohingya, and Rakhine ethnicities (mean age, 23.8 years; male, 96%) had symmetrical, ascending areflexic weakness with at least one additional presenting symptom of fever, lower limb swelling, vomiting, abdominal pain, or difficulty in breathing. Twenty (83.3%) had sensory symptoms. Ten (41.6%) had cranial nerve involvement. Nineteen patients had cerebrospinal fluid examinations but none with evidence of albuminocytological dissociation. Neurophysiological assessment revealed axonal polyneuropathy, predominantly a motor-sensory subtype. Folate and vitamin B12 deficiencies were detected in 31.5% of them. These findings suggested the presence of a polyneuropathy related to nutrition against a backdrop of other possible environmental factors such as infections, metabolic disorders, or exposure to unknown toxin. Supportive treatment with appropriate vitamins supplementation improved functional outcome in most patients. Conclusion. We report a spectrum of acquired reversible neurological manifestations among Myanmarese refugees likely to be multifactorial with micronutrient deficiencies playing an important role in the pathogenesis.

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Reversible isolated sensory axonal neuropathy due to cobalamin deficiency

Cited by 15 publications

References 18 publications

Rapid healing of a patient with dramatic subacute combined degeneration of spinal cord: a case report

Rapid healing of a patient with dramatic subacute combined degeneration of spinal cord: a case report

A Case of Significant Malnutrition Presenting as Acute Sensorimotor Axonal Neuropathy

Myanmarese Neuropathy: Clinical Description of Acute Peripheral Neuropathy Detected among Myanmarese Refugees in Malaysia

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