Polyneuropathies are multifactorial disorders, frequently encountered in practice, characterized by lower motor tetraparesis/-plegia with or without cranial nerve deficits.
This report presents the diagnostic investigation of 5 canine polyneuropathy cases, selected out of a 16-caseload (2016).
Five male dogs were presented with flaccid tetraparesis (2/5), tetraplegia (2/5) or abnormal gait (1/5). Onset of signs was acute (4/5) or subacute (1/5). Dysphonia (3/5) and dysphagia (1/5) were also noted. Neurologic examination revealed generalized weakness (4/5), flaccid tetraparesis (2/5) and tetraplegia (2/5), carpal laxity (1/5), depression (1/5), generalized (2/3) or localized (1/3) muscle atrophy. Proprioception deficits (2/5), hyporeflexia (4/5) and laryngeal paresis (1/5) were noted. Anti-acetylcholine receptor antibody titer (2/2), thyroid function testing (2/2) and cerebrospinal fluid analysis (2/2) were normal. Serology for Toxoplasma gondii IgM (1/1) and snap test for Leishmania infantum (2/3) were negative. Electromyography revealed diffuse spontaneous electrical activity (4/4). Wet biopsy of muscle (cryohistology) revealed chronic denervation muscle atrophy (5/5), lymphoplasmacytic (1/5) or lymphohistiocytic (1/5) chronic interstitial myositis, chronic axonal neuropathy (1/5) or diffuse lymphoplasmacytic neuritis/perineuritis (1/5).
Treatment consisted of physiotherapy (5/5), intensive care and mechanical ventilation (1/5), gabapentin (1/5), clindamycin (2/5), prednisolone (1/5). One dog died of respiratory paralysis, one was euthanased, while 2 remained stable and one improved during follow up.
Polyneuropathies should be differentiated by myopathies and junctionopathies or focal myelopathies. Wet muscle biopsy allows for assessment of myofibre enzyme activities, muscle fibrils, mitochondria, denervation atrophy and pathological storage of polysaccharides and lipids. Nevertheless, the gold standard for diagnosing polyneuropathies is nerve biopsy.