Chronic Tension-type Headache with Vitamin D Deficiency: Casual or Causal Association?

Sanjay Prakash, DM; Nilima D. Shah, MD

Disclosures

Headache. 2009;49(8):1214-1222. 

In This Article

Case Reports

We observed 8 patients over a period of 1.5 years. Three patients are described in detail. Written informed consent was taken from the patients to publish this report.

Case 1

A 42-year-old man had a 2- to 3-year history of episodic headache. The headache was described as dull, holocephalic, and as mild for most of the time. However, occasional exacerbations occurred, escalating to moderate to severe intensity. Photophobia, phonophobia, nausea, or vomiting was never reported. Physical exercise did not worsen the headache. Stress and sleep deprivation were noted as triggering factors. The frequency was 5–6 times per month in early part of the illness. However, it increased to more than 15 times per month in the last 10 months. The duration of an episode ranged from a few hours to few days. General and neurological examinations were normal. Magnetic resonance imaging (MRI) did not reveal any abnormality. Routine biochemical examinations were normal. A diagnosis of CTTH was made. We advised amitryptiline (75 mg daily) as preventive therapy and naproxen (500 mg) as abortive therapy. In the next 6–7 months, he did not feel any improvement in the headache frequency and intensity. In fact, he noted development of new symptoms. The patient started to experience pain in the back and both lower limbs (LL). He also complained of difficulty in climbing stairs and getting up from a sitting posture. He had curtailed his physical activity because of easy fatigability. Repeat neurological examination revealed quadriparesis (especially proximal muscle) with normal muscle bulk and deep tendon reflexes. Sensation was intact and gait was unremarkable. There was generalized muscle tenderness (including pericranial muscle). Bone tenderness was noted on the tibia, femur, humerus, ulna, and skull. A working diagnosis of osteomalacia (with myopathy) was made and the patient was subjected to various investigations. A skeletal X-ray showed demineralization and Looser's zone (pseudofracture). Serum (total) calcium was 7.8 mg/100 mL (normal 8.5–10.5 mg/dL), serum calcium (ionized) was 3.8 mg/100 mL (4.5–5.6 mg/dL), serum phosphate 2.2 mg/100 mL (3–4.5 mg/dL), serum alkaline phosphatase 264 IU/L (30–120 IU/L), 25-hydroxy vitamin D [25(OH) D] 5 ng/mL (> 20 ng/mL), serum parathyroid hormone (PTH) 162 pg/mL (10–60 pg/mL), serum creatine kinase phosphokinase (CPK) 212 U/L (25–200 U/L). Electromyography (EMG) showed short and low muscle action potential (MUAP), polyphasic MUAP, and early recruitment. Other routine hematological and biochemical examinations were normal. Muscle and bone biopsy were not done. The cause of vitamin D deficiency (osteomalacia) was not evident, and it was considered nutritional in origin. The patient was treated with vitamin D3 (1500 IU/day) with calcium supplementation (1500 mg/day). Naproxen (500 mg) was advised as abortive therapy for severe body or head pain. Within 2 weeks the head and body pain started to improve. His headache subsided completely in 4 weeks. Body pain subsided in about 6 weeks. Motor weakness improved to near normal in 4 months. However, mild bone tenderness was present up to 6 months after the initiation of vitamin D and calcium therapy. Repeat vitamin D level was normal after 4 months.

Case 2

A 51-year-old woman presented with about 1-year history of headache. She described the headache as holocephalic and continuous since the onset. It was felt as mild for most of the times; occasional exacerbations occurred, escalating to moderate to severe intensity (occasionally requiring bed rest) for a few hours. However, the exacerbations (pain intensity) did not get worse with her routine physical activities. The frequency of exacerbation was 1–2 times per month in the early part of the illness. However, it increased to about 3–4 times per week for the last few months. The headache was never pulsatile in nature, even when the severity increased. The patient denied the presence of nausea, vomiting, photophobia, phonophobia, auras, or any cranial autonomic features even during the exacerbation phase. Prior treatment with amitryptiline, dothiepin, duloxetine, propranolol, topiramate, ibuprofen, naproxen, indomethacin, etc, produced minimal or no effect.

On direct questioning, she admitted having intermittent muscle aches, especially of the low back, hip, LL, and both shoulders for the last few months. She denied the presence of any muscle weakness. However, she had curtailed her physical activities because of easy fatigability.

Neurological examination revealed symmetrical proximal muscles (of LL) with normal muscle bulk. All deep tendon reflexes were brisk, and the plantar responses were flexor. Sensation was normal. There was generalized muscle tenderness (including pericranial muscle). Bone tenderness was noted on the femur, humerus, and ulna.

A diagnosis of CTTH and osteomalacia was made. MRI of the brain was normal. Radiological examination of the skeleton showed generalized loss of bone density. Serum (total) calcium was 7.2 mg/100 mL, serum (ionized) calcium (2.8 mg/dL), serum phosphate 2.2 mg/100 mL, serum alkaline phosphatase 264 IU/L, and vitamin D (25[OH] D) 8 ng/mL. EMG confirmed myopathy. Other routine hematological and biochemical examinations (including CPK) were normal. Muscle and bone biopsies were not performed. Vitamin D deficiency was probably due to undernutrition as there was no other obvious cause for it.

The patient was treated with vitamin D (1500 IU/day) with calcium supplementation (1500 mg/day). Within a few weeks of commencing the treatment her headache started to improve. The headache and spontaneous muscle pain subsided completely in about 6 weeks' duration. The bone tenderness reduced markedly in about 3 months' duration. Vitamin D level returned to normal after 3 months.

Case 3

A 54-year-old woman presented complaining of progressive lethargy, easy fatigability, diffuse body pain, and weakness of all 4 limbs. The patient also began to complain of low back and hip pain for about 2–3 years prior to presentation. Initially pain was intermittent (for a few hours) and was attributed mainly to overwork or excessive physical activities. The muscle pain intensity, frequency, and duration progressed over time. She gradually curtailed her physical activity. She had tried over the counter pain medications without much help. About 6 months before the presentation, the patient started to experience difficulty in climbing stairs, getting up from a sitting position or from bed, and in lifting heavy objects.

On direct questioning, she admitted having headaches for about 10 months. Mild pressing type feeling in scalp was perceived throughout the day over the last few months. There were occasional (4–6 times per month) superimposed exacerbations of moderate to severe intensity. The duration of exacerbations varied from a few minutes to 1 day. Headache was never throbbing in the nature. No photophobia, phonophobia, nausea, or vomiting were reported. Routine activities did not worsen her headache.

Physical and neurological examinations were normal except for the presence of proximal muscle weakness and diffuse muscle tenderness (including pericranial muscle). Bone tenderness was present with very mild pressure on the tibia, humerus, ulna, and sternum.

A skeletal X-ray showed evidence of osteomalacia. Serum (total) calcium was 7.2 mg/100 mL, serum phosphate 2.2 mg/100 mL, serum alkaline phosphatase 264 IU/L, 24-hour urinary calcium excretion 76 mg, and vitamin D (25[OH] D) 8 ng/mL, serum CPK 298 mg/dL. EMG confirmed myopathy. Other hematological and biochemical examinations were normal. Muscle and bone biopsy were not done. The cause of vitamin D deficiency (osteomalacia) was not evident, and it was considered due to undernutrition.

The patient was treated with vitamin D (1500 IU/day) with calcium supplementation (1000 mg/day). The headache subsided completely in about 4 weeks' duration. Six weeks later, the diffuse body pain disappeared completely. Muscle strength and bone tenderness improved markedly in 4 months' duration. Vitamin D level returned to normal level.

The salient features of other 5 cases are summarized in the Table. All cases fulfilled the criteria for CTTH. No cases had associated headache symptoms such as aura, nausea, vomiting, photophobia, phonophobia, etc. All patients had history of easy fatigability. The neurological examination was normal except for the presence of proximal muscle weakness (in all 5 patients). All cases had muscle tenderness (including pericranial muscle). Neuroimaging (MRI Brain) did not reveal any abnormality.

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