More information about text formats
Thank you for your interest in our case report.
To address your first point, we did not carry out nerve conduction studies or electromyography. The patient was seen as a part of a hyperacute stroke service and we made the diagnosis within 48 hours of symptom onset. After finding an explanatory central lesion, we did not look further peripherally. It would seem to be highly unlikely the patient had developed a simultaneous acute stroke in a relevant area of cortex and peroneal nerve lesion. It is interesting you mention teaching medical students in your response - we teach our students about Occam's razor! As you will no doubt be aware, neurophysiology conducted this soon after symptom onset will be unlikely to contribute in any case, and we are not in the habit of recalling patients at a later date for additional investigations for purely academic value, and we are sure many would share our view this is not appropriate given the current pressure the NHS is under. A stroke diagnosis changes management in terms of secondary preventative medications, hypothetically diagnosing a co-existent compressive neuropathy does not add.
Secondly, we would argue that the location of this lesion does explain the neurological signs quite satisfactorily. As we know, the ankle dorsiflexors are in fact located in the anterior compartment of the lower leg, just below the knee and not actually in the foot itself. Furthermore, there is likely to be considerable individual var...
Secondly, we would argue that the location of this lesion does explain the neurological signs quite satisfactorily. As we know, the ankle dorsiflexors are in fact located in the anterior compartment of the lower leg, just below the knee and not actually in the foot itself. Furthermore, there is likely to be considerable individual variation in precise cortical areas where individual muscles are represented - to quote Penfield's original paper from which the homunculus is derived - "we do not know what the architectural pattern is in any particular case and how much these boundaries may vary from individual to individual", indeed they stated that between "different individuals the result will vary greatly so that any standardized chart which localizes the position of those points upon the cortex may be correct for one individual but not for all" (1).
Robin Fox and Laszlo Sztriha
Letter to the editor; 14th February 2021
RE: Cortical foot
Fox R,Sztriha L. Pract Neurol 2021, 21:73-74
We read the above article (like all highly educational articles of Practical Neurology) with interest.
As the authors pointed out the clinical picture is highly suggestive of peroneal nerve lesion. There was no mention of NCS and EMG had been undertaken in this case. If NCS were carried out then it is prudent to stated that Nerve Conduction Studies excluded Common Peroneal nerve lesion, to make the case water tight and credible.
It is known that elderly would wake up with foot drop due to Peroneal nerve lesion and not necessarily indicate a stroke. In this case an ischaemic lesion was noted at the top of the motor strip and not in the depth of central sulcus where the foot is located. As the homunculus illustrates in Figure 2, the lesion is at the Knee area at best). Parasagittal meningiomas in the depth cause the foot weakness(also suggesting that the well-known ‘homunculus illustration is probably accurate’!) and we teach medical students practical neuroanatomy and localization using such examples. Thus it would be helpful for the paper to document all claims as accurately as possible.
Dr S Wimalaratna, Neurologist, Kettering General Hospital
Dr S Alagoda, Clinical Neurophysiologist, Musgrove Park Hospital, Taunton