Gait Dyspraxia due to Right Occipital Infarct

Dear Editor, A 61-year-old male patient with a history of diabetes mellitus, hypertension and Hodgkin’s lymphoma (in remission over the last 20 years) was admitted due to visual disturbances and gait impairment which began abruptly 6 hours ago. On neurological examination, the patient was oriented and cooperated. Motor, sensory and cerebellar examinations were normal. However, a left-sided partial visual-field defect was apparent. In addition, gait difficulty (compatible with gait dyspraxia) was identified while he was walking. Cranial MRI showed diffusion restriction in the right occipital lobe (Figure 1). Laboratory investigations were unremarkable (hemogram, biochemistry, low-density lipoprotein: 67 mg/dL). Further investigations including brain/neck tomography angiography, echocardiography and 24-hourrhythm Holter were normal. With the diagnosis of cryptogenic stroke, the patient was discharged on aspirin therapy. On the sixth month of follow up at the polyclinic visit, the patient still suffered from gait difficulty and balance problems. He had experienced falling backwards several times since discharge. On neurological examination, a broad-based, cautious walking pattern was observed (Supplementary Video 1 in the online-only Data Supplement). In addition, postural instability was apparent such that the patient scored a 2 (would fall if not caught) on the Nutt retropulsion test (Supplementary Video 2 in the online-only Data Supplement). 1 Confrontation visual field testing showed a bilateral normal visual field. Of note, for the investigation of visuoconstructive function, a clock drawing test was performed, which was normal. In addition, the Wechsler memory index (WMI)-IV (Visual Reproduction I subitem) was also performed, which was evaluated at 5/14 points (within the normal range, when normalized for age and education). He was referred to physical therapy for an intensive physical therapy program of proprioceptive and balance exercises. Gait dyspraxia can be defined as a type of gait abnormality that cannot be explained by a demonstrable deficit in pyramidal, extrapyramidal, sensory, or cerebellar systems.2 Gait dyspraxia is generally used to define the abnormal gait that accompanies cerebral small vessel disease, normal pressure hydrocephalus and some frontal lobe disorders. Based on the affected neuroanatomical regions and responsible pathophysiological mechanisms, Nutt3 recently suggested a classification of two subtypes: anterior and posterior higher-level gait disorders (HLGD). We think that this index case represents a smart presentation of a patient with posterior HLGD. However, the reporting of cases with isolated gait dyspraxia following acute stroke (as in our case) is extremely rare in the literature.4 Furthermore, the lesion site in the cuneus in our case was considerably localized providing substantial perspective on the clear role of this anatomical localization in locomotion. The cuneus is generally known for its involvement in basic visual processing. Considering that locomotion is a task that unarguably requires visuospatial processing, the mechanisms relating the outcome to the injury localization can be understood. On the other hand, the clock drawing test and WMIIV-Visual Reproduction I tests were in the normal ranges, which does not support the abovementioned hypothesis. However, we think that these cognitive tests might have failed to detect a mild deterioration in visuospatial function because they are not highly sensitive tests. Of note, and in accordance with this thought, the patient and his relatives had stated that he had significant difficulty performing these tests in his premorbid state. In the literature, the posterior parietal cortex and visuospatial attention have been repeatedly emphasized as critical for the execution of loco-