Ganga-Meghna Brahmaputra || West Bengal || Bangladesh || Middle Ganga Plain, Bihar || Uttarpradesh
Jharkhand || North-East Hilly States || Rajnandgaon, Chattisgarh || Behala, Kolkata, WB || As toxicity- Homeopathic Treatment
Effectiveness & Reliability - As Field Testing Kits || Utility Of Treatment Plant
Causes, Effects & Remedies - Groundwater As Calamity || References

Arsenic Poisoning in Bihar : Environmental Health

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NEUROLOGICAL INVOLVEMENT IN PATIENTS OF ARSENICOSIS

The obvious frequency of disabling neurologic signs initiated a more detailed examination and comparison with neuropathy found in arsenic affected areas of West Bengal (Chakraborti et al. 1999a; Chowdhury et al. 2000a, 2000b; Rahman et al. 2001). Of the 60 index subjects with skin lesions, a convenience sample of 40 (32 adults: 20 M, 12 F; 8 children 8–15 years: 5 M, 3 F) underwent a detailed neurological examination by the same neurologist (SCM) of earlier studies (Chakraborti et al. 1999a; Chowdhury et al. 2000a; 2000b; Rahman et al. 2001). Observations were recorded for items considered consistent with peripheral motor and sensory neuropathy and for other neurologic observations [as modified from Feldman et al. (1979), Galer (1998), and Kreiss et al. (1983)]. Items included to characterize neuropathy were (i) pain and paraesthesias (e.g. burning) in a stocking and glove?distribution, (ii) numbness, (iii) hyperpathia/allodynia, (iv) distal hypesthesias (reduced perception of sensation to pinprick/reduced or absent vibratory perception/affected joint position sensation/affected touch sensation), (v) calf tenderness, (vi) weakness/atrophy of distal limb muscles or gait disorder, (vii) reduction or absence of tendon reflexes.

Neurologic Findings

Arsenic neuropathy was clinically diagnosed in 21 (52.5%) of the 40 cases examined based on our previously defined criteria (Feldman et al. 1979; Galer 1998; Kreiss et al. 1983; Rahman et al. 2001). They all had arsenical skin lesions and elevated levels of arsenic in the hair, nail, and urine and in the drinking water (range 202 to 1654 µg/L). Table 3 shows arsenic concentration in urine, hair and nail of some patients and non-patients from Semria Ojha Patti village. The normal range of arsenic in biological samples is as cited in Table 3. Alternative causes excluded were inflammatory (Guillain Barre Syndrome), metabolic, nutritional, infectious, malignancy associated, hereditary, physical agents, entrapment, alcoholic, other toxins, and drugs. Two cases of arsenicosis who had mononeuritis multiplex due to leprosy were excluded. The major presenting features are shown in Table 4. Most of the cases presented with distal paresthesias (40%) and distal hypoesthesias (35%) in stocking and glove distribution followed by limb pains and diminished or absent tendon reflexes (each 12.5%). Muscle weakness and atrophy affected only 3 patients (7.5%). Obvious signs of autonomic instability, cranial nerve involvement, headache, vertigo, sleep disorder, and mental changes were conspicuous by their absence. One 60-year-old woman had developed paranoid psychosis requiring treatment following the appearance of florid arsenical skin lesions, but this was not included in the tabulation.

Frequency of Neuropathy?

The prevalence of neuropathy in this sample was 21/40 or 52.5% (Table 4), with males less affected (10/25; 40%) than females (11/15; 73.3%). Only 1 of 8 children (6–15 years) was affected (12.5%). The prevalence in males over 15 years of age was 62.5% and in females over 15 was 84.6%.

Type and Severity of Neuropathy

Table 4 lists 18 cases (45%) of sensory neuropathy while 3 cases (7.5%) had motor components as well (sensorimotor type). Moderate neuropathy was evident in 4 (10%). This was based on rigorous criteria of neuropathy (Kreiss et al. 1983) and included cases with impairment of at least 2 sensory modalities and reduced deep tendon reflexes. The remaining 17 cases (42.5%) had mild (predominantly sensory) neuropathy.

Magnitude of Neurological Involvement and Comparative Analysis

The reported prevalence of neuropathy in arsenic toxicity from chronic low dose exposure to arsenic contaminated water or occupational sources ranged from as low as 8.8% to 32% (Kreiss et al. 1983; Hotta 1989). Our own studies of large numbers of arsenicosis patients in West Bengal disclosed neuropathy in 34–37% (Chakraborti et al. 1999a; Chowdhury et al. 2000a, 2000b; Mukherjee et al. 2003; Rahman et al. 2001) except for a small population of subacute as opposed to chronic exposure where we found 86.8% (Rahman et al. 2001).

Relationship of Neuropathy and Arsenic Consumption

The 4 patients with moderate and sensorimotor neuropathy utilized water with arsenic 750 µg/L and above; the 13 patients with mild and predominantly sensory neuropathy consumed water with arsenic 207 µg/L to 637 µg/L.

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