Pseudoperipheral palsy: a case of subcortical infarction imitating peripheral neuropathy

It is known that pure motor nerve deficits resulting from acute stroke can occur in the central hand control network [2], but also angular gyrus [4], the ventroposterolateral nuclei of thalamus [5], internal capsule, corona radiate, pontine base and/or ventromedial medulla. It is hypothesised that discrete functional cortical areas for each finger exist and are sequentially arranged [6], which means that finger movements are controlled by a highly distributed network rather than by functionally and spatially discrete groups of neurons controlling each finger [7]. This is also supported by the findings of one study, in which none of the patients showed hand motor deficits limited strictly to one or a few fingers, but rather both radial and ulnar sided hand motor deficits in varying degrees. The authors suggested this to be a characteristic form of finger motor deficits due to a cortical lesion which is important to differentiate the clinical picture from lesions at other locations [8]. Clinicoradiological signs observed in our patient exhibiting pseudoperipheral neuropathy due to small subcortical infarction well support motor hand area in the motor homunculus in the hand area.

With a muscle hand atrophy, one should also look for compression of the ventral roots or of the anterior horns of grey matter in the cervical regions. The muscle atrophy in such cases is due to a longstanding lower motor neuron lesion and is often accompanied by weakness and fasciculation of the muscles innervated by the affected segments. No radiological evidence for cervical compression was found in our patient.

Functional MRI techniques suggest that the hand knob area, which controls hand motor function [9], is located in the posterior part of the precentral gyrus, near the central sulcus [9‐11].

CT of the brain is often insufficient to diagnose the majority of ischemic lesions in the hand knob area, mostly due to the small lesional size and the subcortical location. Diffusion-weighted MRI is more sensitive to confirm the involvement of the precentral knob, and should be included as part of the standard evaluation. The treatment of an infarct in the hand knob area is dependent of the suspected etiology, ranging from arterio-arterial embolism to atherosclerotic infarcts [12]. However, little is known about the underlying pathological mechanisms of this stroke entity [12].

Diagnosis of cerebral angiitis is challenging. Brain biopsy remains the gold standard [13]; however, positive DSA, MRI and cerebrospinal fluid findings are sufficient to diagnose «probable» cerebral angiitis [13, 14]. Recent 3-Tesla MRI studies using increased magnetic field strengths have identified distinct vasculitic patterns, with arterial wall thickening and enhancement in both proximal and distal small intracranial vessels [15‐17], that can remain stable for more than 12 months (median follow-up 13.5 months) [16]. 3-Tesla MRI to detect arterial wall inflammation may therefore become the favored criterion for diagnosing cerebral angiitis [17]. Nevertheless, other causes of arterial wall enhancement (e.g., atherosclerosis, radiation vasculopathy, infection, and vasospasm) must be excluded, and studies in a wider range of disorders are required to properly define the role of 3-Tesla MRI in the diagnostic process [17]. It is also possible that our patient had pseudoperipheral palsy due to cerebral angiitis, which was not detected by routine nerve conduction studies.

Although long-term data are scarce, the early-phase prognosis of similar cases is typically good [12], possibly due to the functions carried out by the damaged cortical area being resumed via the recruitment of adjacent areas [18].