Functional neuroimaging research has consistently associated brain structures within the default mode network (DMN) and frontoparietal network (FPN) with mind‐wandering. Targeted lesion research has documented impairments in mind‐wandering after damage to the medial prefrontal cortex (mPFC) and hippocampal regions associated with the DMN. However, no lesion studies to date have applied lesion network mapping to identify common networks associated with deficits in mind‐wandering. In lesion network mapping, resting‐state functional connectivity data from healthy participants are used to infer which brain regions are functionally connected to each lesion location from a sample with brain injury. In the current study, we conducted a lesion network mapping analysis to test the hypothesis that lesions affecting the DMN and FPN would be associated with diminished mind‐wandering. We assessed mind‐wandering frequency on the Imaginal Processes Inventory (IPI) in participants with brain injury (n = 29) and healthy comparison participants without brain injury (n = 19). Lesion network mapping analyses showed the strongest association of reduced mind‐wandering with the left inferior parietal lobule within the DMN. In addition, traditional lesion symptom mapping results revealed that reduced mind‐wandering was associated with lesions of the dorsal, ventral, and anterior sectors of mPFC, parietal lobule, and inferior frontal gyrus in the DMN (p < 0.05 uncorrected). These findings provide novel lesion support for the role of the DMN in mind‐wandering and contribute to a burgeoning literature on the neural correlates of spontaneous cognition.

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BACKGROUND Chiari Malformation Type I (CM-I) is defined as cerebellar tonsil displacement more than 5 mm below the foramen magnum. This displacement can alter cerebrospinal fluid flow at the cervicomedullary junction resulting in Valsalva-induced headaches and syringomyelia and compress the brainstem resulting in bulbar symptoms. However, little is known about cognitive and psychological changes in CM-I. OBJECTIVE To prospectively assess cognitive and psychological performance in CM-I and determine whether changes occur after surgical decompression. METHODS Blinded evaluators assessed symptomatic CM-I patients ages ≥18 with a battery of neuropsychological and psychological tests. Testing was conducted preoperatively and 6 to 18 mo postoperatively. Data were converted to Z-scores based on normative data, and t-tests were used to analyze pre-post changes. RESULTS A total of 26 patients were included, with 19 completing both pre- and post-op cognitive assessments. All patients had resolution of Valsalva-induced headaches and there was improvement in swallowing dysfunction (P &lt; .0001), ataxia (P = .008), and sleep apnea (P = .021). Baseline performances in visual perception and construction (z = −1.11, P = .001) and visuospatial memory (z = −0.93, P = .002) were below average. Pre-post comparisons showed that CM-I patients had stable cognitive and psychological functioning after surgery, without significant changes from preoperative levels. CONCLUSION CM-I patients had below average performance in visuospatial and visuoconstructional abilities preoperatively. Prospective longitudinal data following surgery demonstrated improved neurologic status without any decline in cognition or psychological functioning. Routine pre- and postoperative formal neuropsychological assessment in CM-I patients help quantify cognitive and behavioral changes associated with surgical decompression.

Objective: Functional brain networks, which include important “hub” regions, provide important ways to understand recovery after brain damage. One crucial hub previously identified in adult human functional brain networks is in the dorsomedial prefrontal cortex (dmPFC). An open question is whether this hub is vulnerable during development. Method: Here, we describe the neuropsychological and neuroanatomical outcomes of a woman who sustained focal damage to the dmPFC hub from a stroke at age 7. Her rare lesion, acquired early in life and affecting the left dmPFC and underlying white matter, afforded a compelling opportunity for new insights into brain–behavior relationships from a developmental perspective. Results: Cognitive impairment ratings by clinical neuropsychologists showed stable cognition over 2 decades with moderate impairments in personal adjustment and adaptive functioning. The cognitive profile of this childhood-onset case is similar to two previously reported adult-onset cases with similar lesion locations. The results suggest that for the hub we sampled with these cases (midline dmPFC), cognitive and behavioral outcomes do not differ for childhood-onset versus adult-onset brain damage, as in both instances there were long-lasting moderate to severe impairments in personal adjustment and adaptive functioning. Preliminary resting-state fMRI data from the childhood-onset case and one of the adult-onset cases are used to propose future directions for exploring questions of neural plasticity and neurorestoration. Conclusions: This case study provides a rare window into cognitive and neural development following early injury to the dmPFC, enhancing understanding of the complex relationships between age at neurological injury, lesion location, and long-term cognitive and behavioral recovery.

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