Article Text

Download PDFPDF

Pure motor stroke with major involvement of the index finger
  1. M Kobayashi,
  2. M Sonoo,
  3. T Shimizu
  1. Department of Neurology, Teikyo University School of Medicine, Tokyo, Japan
  1. Correspondence to:
 M Sonoo
 Department of Neurology, Teikyo University School of Medicine, Kaga 2–11–1, Itabashi-ku, Tokyo 173, Japan;

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

A selective weakness of a particular group of fingers due to cortical infarction has been reported by several authors.1–3 This finding is related to the controversy over the somatotopic organization of the primary motor cortex (M1). Traditionally, a discrete somatotopic arrangement for individual fingers, with the radial fingers represented laterally and the ulnar fingers medially, has been assumed. However, recent theories have suggested functional overlapping of the cortical representation of the fingers. We describe here a case presenting with major weakness of the index finger due to a cortical infarction confirmed by MRI.

Case report

A 71 year old right handed man noted difficulty in using his toothbrush one morning. He complained of weakness in his right index finger and was admitted to our hospital on the day of onset. He had no previous illnesses nor risk for stroke. Neurological examination revealed the following muscle weaknesses: extension, abduction, and adduction of the right index finger (2-/5 as scored by the Medical Research Council (MRC) grading system); radial abduction of the middle finger (3/5); and 4/5 for extension of the middle finger, abduction of the little finger, and flexor digitorum profundus of the index finger. Strength was normal for the other finger movements, including all directions of thumb movement, and wrist, elbow, and shoulder movements were also completely normal. He had no sensory deficits, including no deficit in combined sensations. There was no evidence of apraxia. Deep tendon reflexes were normal; the Babinski sign was negative on both sides. There were no significant laboratory abnormalities, and electrocardiography and echocardiography were normal. Carotid ultrasonography revealed a small plaque echo in the left common carotid artery. Needle EMG of the right first dorsal interosseus muscle, performed on the first day, showed a pattern consistent with central weakness. A brain MRI performed on the fifth day of admission revealed two hyperintense spots in the precentral knob and the subcortical white matter, by both diffusion-weighted and T2-weighted images, indicating an acute ischaemic stroke (fig 1). His symptoms began to improve within one week, and largely resolved in two weeks.

Figure 1

T2-weighted (A) and (D), fluid attenuated inversion recovery (B) and (E), and diffusion weighted (D) and (F) MRI images are shown for the two axial slices. Two small high intensity spots were identified in the precentral knob (A–C) and at the subcortical white matter (D–F).


This case presented with a predominant weakness of the index finger; needle EMG revealed unequivocal central weakness. An MRI demonstrated two acute strokes, in the contralateral subcortical white matter and precentral knob, respectively. However, we suggest that the latter was responsible for the symptoms, in that the precentral knob is associated with the motor hand area.4 In addition, it is difficult to conceive of a mechanism whereby such selective weakness could be caused by a subcortical lesion.

Earlier studies proposed discrete M1 somatotopy for individual finger movements, arranged with the thumb most lateral and the little finger most medial, as illustrated by the renowned homunculus of Penfield.5 However, more recent studies, using either cortical stimulation in monkeys or functional MRI in humans, have mostly demonstrated a dispersed and overlapping representation over a rather wide M1 area for finger and hand movements.

Patients with small cortical lesions can provide additional information on this issue. Several authors have reported examples presenting with predominant weakness of a particular finger or group of fingers; most presented with predominant weakness of either the thumb or the little finger.1,2 Schieber emphasised that they had identified no cases, either in their own experience or in the literature, with the greatest weakness in the index, middle, or ring fingers, and with stronger fingers on either side.1 He also stated that in no instance was a single digit more than one unit on the MRC scale weaker than the other four digits. The only exceptions hitherto may be the two cases reported by Kim2 and Kim et al,3 showing the greatest or isolated weakness in the index finger; but the strength of the index finger was only mildly affected (4/5) in both patients. Therefore, clear evidence for discrete somatotopy for individual fingers is lacking, although a lateromedial gradient in cortical representation for the fingers from the radial to the ulnar side has been suggested.1,2

The present case is unique in presenting with prominent weakness of the index finger (2-/5), sparing the thumb and largely sparing the fingers on the ulnar side. Another interesting feature is the clear dissociation between the weak extension and adduction/abduction movements (2-/5) v the almost preserved flexion (4/5 or 5/5) of the index finger. The classical experiment by Penfield5 indicated that certain cortical points did produce, although rarely, an isolated movement of a single finger. The present result suggests that there is a localised area predominantly responsible for the movement of a single finger, at least for the index finger, as well as for the specific direction of movement.