Distal Radius Fracture Treatment Outcomes in Patients With Ipsilateral Hemiplegia or Hemiparesis

Background Little information exists to guide decision-making with regard to distal radius fractures in the setting of ipsilateral hemiparesis or hemiplegia. Methods Patients who sustained a distal radius fracture in the setting of ipsilateral hemiparesis or hemiplegia secondary to brain injury were evaluated. Investigated variables included perioperative pain, preinjury House functional classification score, length of immobilization, radiographic outcome measurements, and time to union. Results There were 15 patients with distal radius fractures with a mean age of 65.9 years. The mean clinical and radiographic follow-up was 2.8 and 2.9 years, respectively. Wrists were placed into the nonoperative group (NOG, n = 10) and operative group (OG, n = 5). Pain significantly decreased at final follow-up for both groups. Baseline House functional classification scores averaged 1.3 and 1.6 for the NOG and OG, respectively, and were maintained at final follow-up. Length of immobilization for the NOG was 46 days and OG was 37 days, P = .15. Radiographic outcomes at final follow-up in the NOG and OG, respectively, were a mean radial height of 9.3 versus. 11.6 mm, radial inclination of 18.3° versus 22.3°, 4.2° dorsal tilt versus 5.3° volar tilt, and tear drop angle of 45.6° versus 44.5°. There were no significant differences in these measurements. Time to radiographic union averaged 58 days for the NOG and 67 days for the OG, P = .42. There were no revision surgeries. Conclusions Based on this small case series, patients with distal radius fracture and ipsilateral hemiparesis or hemiplegia may have similar clinical, functional, and radiographic outcomes, regardless of nonoperative or operative treatment.

Teaching NeuroImages: All hemiparesis are not contralateral

A 56-yr-old hypertensive male presented with left-sided weakness of 2-h duration. He made complete recovery from right hemiparesis due to left parietal infarct. Examination showed dysarthria and left hemiparesis (NIHSS 8/42). MR-brain showed both left parietal acute infarct and gliosis from old infarct (Figure-1). He was successfully thrombolysed with intravenous alteplase. Present stroke was diagnosed as ipsilateral hemiparesis, confirmed by DTI (Figure-2). Ipsilateral hemiparesis, mostly seen with posterior fossa malformations and remote infarctions, results from injury to uncrossed corticospinal tract (CST) in patients of remote brain injury or with no decussation of CST or injury to ipsilateral extrapyramidal motor pathway.

Ipsilateral hemiparesis: the forgotten history of this paradoxical neurological sign

OBJECTIVEEstablishing the neurological localization doctrine for the contralateral hemispheric control of motor functions in the second half of the 19th century, researchers faced the challenge of recognizing false localizing signs, in particular paradoxical or ipsilateral hemiparesis (IH). Despite tremendous progress in current methods of neuroradiological and electrophysiological exploration, a complete understanding of this phenomenon has yet to be attained.METHODSThe authors researched the well-described cases of hemiparesis/hemiplegia ipsilateral to an intracranial lesion published in the scientific literature in the pre-MRI era (before 1980). A comprehensive review of the physiopathological mechanisms proposed for paradoxical hemiparesis throughout this period, as well as the pathological evidence substantiating them, is provided.RESULTSA collection of 75 patients with hemiparesis/hemiplegia ipsilateral to the primary intracranial lesion reported between 1858 and 1979 were eligible for analysis. Most cases occurred in adults with supratentorial, slowly developing, extraparenchymatous mass lesions, such as neoplasms (38%) or chronic subdural hematomas (36%). Physiopathological theories proposed by the neurologists who investigated IH can be grouped into 4 major concepts: 1) lack of anatomical decussation of the corticospinal tract; 2) impaired functional activation of the contralateral hemisphere by the lesioned dominant hemisphere through the callosal connections; 3) Kernohan’s notch phenomenon, or mechanical injury of the contralateral cerebral peduncle against the free edge of the tentorium; and 4) cerebrovascular dysfunction involving the contralateral hemisphere owing to kinking and mechanical flattening of the carotid artery contralateral to the primary intracranial lesion.CONCLUSIONSIH represents a still underdiagnosed paradoxical neurological phenomenon. With the aid of modern neuroradiological and neurophysiological methods, Kernohan’s peduncle notch mechanism has been confirmed to cause IH in many of the cases reported in recent decades. Nevertheless, alternative functional and/or vascular mechanisms must be investigated further for unexplained IH cases, in particular for transitory IH without evidence of peduncle injury. The historical theories reviewed in this paper represent a conceptual framework that may be helpful for this purpose.