Idiopathic polyneuropathy is an illness with sensory and motor disorders characterized by abnormal sensations of paresthesia, numbness, and pain in the feet and hands. There is no underlying cause for idiopathic polyneuropathy. Additionally, there may be muscle weakness in the feet and hands, problems with balancing, and walking difficulty in the dark or on uneven surfaces. A minority of the autonomic nervous system patients might be involved, and the patients may have vomiting, persistent nausea, diarrhea, incontinence, constipation, sweating, sexual dysfunction, or abnormalities [13].
In the present study, the mean age of idiopathic polyneuropathy (55.8 7.5) years ranged from (45–71) years, with a male-to-female ratio of 55–45%, which provides information on the late onset of idiopathic polyneuropathy in both sexes. These findings are consistent with those of De Sousa [14] and Wolfe et al. [15], who found that the mean age of idiopathic poly neuropathy ranges between 51–63 years, as well as Lindh et al. [16], who found the incidence age is between (40–70) years, with slight female predominance.
In the present study, the age of onset was (52 ± 7) years, ranging between (44–70) years, which explains that patients complain after years from the onset of developing symptoms of neuropathy due to the slow progression, while the duration of illness (3 ± 1.6) years, ranging between (1–6) years and DN4 score is (5.6 ± 0.06) ranging between (5–7), which explains the slowly progressive course of the disease with the inability to diagnose easily because of the presence of these symptoms at old age without neuropathic feature. This finding agrees with Chiaramonte et al. [17], who found that the onset of idiopathic poly neuropathy (47.6 ± 12.6) years and duration of illness is (3.9 ± 3) years, and the DN4 score is 5.
The pain was reported in 60%, sensory loss in 20%, distal weakness in 70%, imbalance in 35%, and autonomic disorder in 25%, with no cranial nerve affection, suggesting that most of the patients had sensory–motor neuropathy without apparent disable weakness. This finding partially agrees with Pasnoor et al. [18], who found pain reported in 27–42%, sensory loss in 65%, distal weakness in 26–82%, and difficulty with balance in 33%.
There are substantial differences between diminished CMAP amplitude (< 0.001) and slow NCV (< 0.001) of both median and ulnar nerves with subclinical involvement of upper limbs despite no obvious abnormal motor findings in clinical examination. This finding is consistent with McLeod et al. [19], who found significant differences between NCV (0.001) and CMAP amplitude (< 0.001) of both median and ulnar nerve in patients with neuropathy of undetermined cause and control groups.
There are significant differences between diminished amplitude (< 0.001) and prolonged DL (0.043) of sensory median nerves and diminished amplitude (< 0.001) and prolonged DL (0.031) of both sensory ulnar nerves, indicating that sensory amplitude is sensitive early to axonal loss owing to collateral reinnervation and with a loss each remaining fiber conduct at its innate speed. Therefore, DL affected the extent of loss, which is compatible with McLeod et al. [19], who found significant differences between prolonged sensory latency (< 0.001) and diminished sensory amplitude (< 0.001) of both median and ulnar nerve in patients with neuropathy of undetermined cause and control groups.
There are significant differences between prolonged DL (< 0.001), diminished CMAP amplitude (< 0.001), and slowing NCV (< 0.001) of both tibial and peroneal nerves as in mild denervation collateral keep the number of muscle fibers high but with further axonal loss greater number of muscle fiber becomes denervated. CMAP amplitude falls and DL and NCV are affected by further degeneration [20], which correspond to the findings of McLeod. et al. [19], who found significant differences between slowing NCV (< 0.001) and diminished CMAP amplitude (< 0.001) of both tibial and peroneal nerves in patients with neuropathy of undetermined cause and control groups.
There is a substantial difference between prolonged LA and diminished amplitude of sural nerves and could be proven with McLeod et al. [19] found significant differences between prolonged sensory latency (0.001) and diminished sensory amplitude (0.001) of both median and ulnar nerve in patients with neuropathy of undetermined cause and control groups as neuropathy characterized by dying back. The phenomenon suggests that the sural nerve is affected earlier and more severely than the sensory upper limbs; consequently, significant differences between sural nerves can be expected.
Abnormal EMG activity was observed in 90% of patients with idiopathic polyneuropathy, and chronic neurogenic findings alone were observed in 60%, chronic neurogenic findings with denervation in 25%, and denervation activity alone in 5%. These results suggest motor axonal injury with evidence of reinnervation in a very slowly progressive course of polyneuropathy [5]. This finding is consistent with Lindh et al. [16] and Nusartha et al. [21], who found that 60% of patients with cryptogenic polyneuropathy had chronic neurogenic findings and 20% had chronic neurogenic findings with denervation. Even if idiopathic polyneuropathy is sensory or sensory–motor, this result suggests that motor nerves are subclinically involved.
In this study, the sensitivity of motor NCS is (47–76) % and sensory NCS (42–83)% and F-wave (46–78)% specificity of motor NCS (72–92) and sensory NCS (73–98) and F-wave (50–95)%. In contrast, Kelmenson et al. [22] found that motor NCS had "a sensitivity of (71–100%) "specificity of (82–96%)" sensory NCS had a sensitivity of (80–100%)" specificity of (31–54%) while Moss et al. [23] illustrated that sensitivity of motor NCS in lower limbs (LL) (88–100%)" specificity (63–85%) while the study in LL had sensitivity (88–100%) specificity (59–81%). The difference in study results is because this study showed the result in both upper and lower limbs.
There are significant differences between prolonged latency SSR (< 0.001) and diminished amplitude SSR (< 0.001) in both hand and foot between patients with idiopathic axonal polyneuropathy and control groups. Consequently, subclinical involvement of small nerve fiber can appear early even in the absence of autonomic symptoms in polyneuropathy [24], which aligns with lin et al. [25], who found significant differences in SSR latency of upper extremity (< 0.05) and amplitude of upper and lower extremity (P < 0.05) between patients with idiopathic axonal neuropathy and control groups.
In this research, sympathetic skin response in diagnosing autonomic neuropathy in patients with idiopathic polyneuropathy had sensitivity (81–89.5) % and specificity (80–86) %, which is compatible with Al-Moallem et al. [26] who found that SSR had a sensitivity of 87.5% and specificity 88.2% in diagnosing idiopathic sensory neuropathy and this could explain the presence of subclinical autonomic involvement even in absence autonomic symptoms.
There is a significant reduction of intraepidermal nerve fiber density at the distal leg (P < 0.001) between patients with chronic idiopathic polyneuropathy and control groups demonstrating selective degeneration of somatic unmyelinated nerve fibers conveying pain and thermal sensation cannot be observed in routine neurophysiological tests [27], aligning with Pittenger et al. [28] who found a significant reduction in IENF (P < 0.001) when comparing control subjects and patients groups in the distal leg of the patients with axonal polyneuropathy.
In this study, the sensitivity of IENFD in diagnosing CIAP is 92.5%, and specificity is 97.5%, indicating that the intra-epidermal nerve fiber density is a more reliable and sensitive factor in diagnosing neuropathy in patients who had little clinical and neurophysiological evidence of neuropathy [29]. This finding corresponds to the results obtained by Devigili et al. [30] and [31], who found that the sensitivity of IENF is 88% specificity is 89% in diagnosing idiopathic sensory polyneuropathy. In addition, it agrees with Chin et al. [32], who stated that IENF has a specificity of 95% and sensitivity of 80%.