Question:
A patient presents with memory loss and clinical features suggestive of subacute combined degeneration (SACD) of the spinal cord. What is the most likely diagnosis?
A patient presents with memory loss and clinical features suggestive of subacute combined degeneration (SACD) of the spinal cord. What is the most likely diagnosis?
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If a patient has severe megaloblastic anemia and neurological signs, treating with Folic Acid (B9) alone will correct the anemia but allow the irreversible neurological damage of B12 deficiency to progress unchecked. Always rule out or concurrently treat B12 deficiency.
Updated On: Sep 3, 2026
- Vitamin B12 deficiency
- Vitamin E deficiency
- Multiple sclerosis
- Friedreich’s ataxia
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The Correct Option is A
Solution and Explanation
Concept:
Subacute Combined Degeneration (SACD) of the spinal cord is a highly specific neurological syndrome involving the simultaneous demyelination of multiple specific tracts within the spinal cord.
The question asks to identify the definitive underlying metabolic cause for this specific neurodegenerative pattern, especially when combined with cognitive symptoms (memory loss).
Explanation:
• Subacute Combined Degeneration is essentially pathognomonic for severe Vitamin B12 (cobalamin) deficiency.
• Vitamin B12 is a required cofactor for the enzyme methionine synthase, which is necessary for the production of S-adenosylmethionine (SAM). SAM is a critical methyl donor required for the synthesis and maintenance of myelin sheaths.
• In B12 deficiency, impaired methylation leads to progressive demyelination. "Combined" refers to the involvement of two major spinal cord tracts:
1. The Dorsal Columns: resulting in loss of proprioception, vibration sense, and sensory ataxia.
2. The Lateral Corticospinal Tracts: resulting in upper motor neuron signs (spastic weakness, positive Babinski sign).
• Furthermore, Vitamin B12 deficiency causes significant cerebral manifestations, frequently presenting with neuropsychiatric symptoms, cognitive slowing, dementia, or profound memory loss.
• Option (B), Vitamin E deficiency, closely mimics SACD in the spinal cord, but it typically does NOT cause the prominent cortical cognitive impairment (memory loss) or the macrocytic anemia seen in B12 deficiency.
• Option (C), Multiple sclerosis, causes patchy, asymmetric demyelinating plaques separated in time and space, rather than the specific, symmetric "combined" tract degeneration of SACD.
• Option (D), Friedreich's ataxia, is a genetic disorder causing spinocerebellar degeneration and hypertrophic cardiomyopathy, typically presenting in early adolescence, unrelated to the memory loss described here.
Final answer:
The specific syndrome of SACD combined with memory loss is the hallmark neurological presentation of Vitamin B12 deficiency.
Subacute Combined Degeneration (SACD) of the spinal cord is a highly specific neurological syndrome involving the simultaneous demyelination of multiple specific tracts within the spinal cord.
The question asks to identify the definitive underlying metabolic cause for this specific neurodegenerative pattern, especially when combined with cognitive symptoms (memory loss).
Explanation:
• Subacute Combined Degeneration is essentially pathognomonic for severe Vitamin B12 (cobalamin) deficiency.
• Vitamin B12 is a required cofactor for the enzyme methionine synthase, which is necessary for the production of S-adenosylmethionine (SAM). SAM is a critical methyl donor required for the synthesis and maintenance of myelin sheaths.
• In B12 deficiency, impaired methylation leads to progressive demyelination. "Combined" refers to the involvement of two major spinal cord tracts:
1. The Dorsal Columns: resulting in loss of proprioception, vibration sense, and sensory ataxia.
2. The Lateral Corticospinal Tracts: resulting in upper motor neuron signs (spastic weakness, positive Babinski sign).
• Furthermore, Vitamin B12 deficiency causes significant cerebral manifestations, frequently presenting with neuropsychiatric symptoms, cognitive slowing, dementia, or profound memory loss.
• Option (B), Vitamin E deficiency, closely mimics SACD in the spinal cord, but it typically does NOT cause the prominent cortical cognitive impairment (memory loss) or the macrocytic anemia seen in B12 deficiency.
• Option (C), Multiple sclerosis, causes patchy, asymmetric demyelinating plaques separated in time and space, rather than the specific, symmetric "combined" tract degeneration of SACD.
• Option (D), Friedreich's ataxia, is a genetic disorder causing spinocerebellar degeneration and hypertrophic cardiomyopathy, typically presenting in early adolescence, unrelated to the memory loss described here.
Final answer:
The specific syndrome of SACD combined with memory loss is the hallmark neurological presentation of Vitamin B12 deficiency.
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