A precentral arteriovenous malformation (AVM) refers to an abnormal tangle of arteries and veins located in or near the precentral gyrus, which is the region of the brain responsible for voluntary motor control (also known as the primary motor cortex).
1. Location Precentral gyrus, anterior to the central sulcus.
Contains the primary motor cortex, which controls contralateral voluntary movement—especially of the face, upper limbs, and lower limbs depending on the somatotopic distribution.
2. Clinical Presentation
Seizures (focal motor), especially if cortical irritation occurs.
Progressive motor deficits, weakness, or hemiparesis if the AVM causes mass effect or hemorrhage.
Intracerebral hemorrhage: common initial presentation in young patients.
3. Imaging
MRI + MRA: detailed localization and relationship with eloquent cortex.
Digital Subtraction Angiography (DSA): gold standard for vascular architecture, nidus size, feeders, and drainers.
4. Treatment Considerations
Complex due to eloquent cortex involvement.
Options include:
Microsurgical resection: risky in eloquent areas; reserved for small, superficial AVMs.
Stereotactic radiosurgery: often preferred for small-to-medium AVMs in motor cortex.
Endovascular embolization: typically adjunctive.
Risk of postoperative motor deficits must be weighed against hemorrhage risk.
5. Functional Mapping
Intraoperative motor evoked potentials (MEPs) and cortical mapping are crucial in surgery.
Navigated TMS and fMRI may aid preoperative planning.
In a retrospective observational case-control study using neuroimaging volumetric analysis Gokoglu et al. from the Erciyes Medical School. Kayseri System Hospital, Vocational Health School, Cappadocia University, NevĹźehir, Department of Neurosurgery, Bezmialem Vakif University, Ä°stanbul published in Revista NeurocirugĂa 1) to determine whether cerebral arteriovenous malformations (AVMs) located in the precentral and postcentral gyri are associated with volumetric changes in other brain structures — both near and remote — using advanced MRI-based analysis:
The authors attempt to attribute widespread volumetric brain changes to AVMs located in a highly focal cortical region. While neuroplasticity and diaschisis are known phenomena, this sweeping claim of remote structural reorganization is insufficiently justified. The title itself sets the tone for an overgeneralized hypothesis masquerading as discovery.
Key details about patient selection, AVM size, Spetzler-Martin grade, hemorrhagic history, or eloquence of surrounding cortex are absent. Were the AVMs ruptured or not? Were the MRIs taken before or after seizure onset, steroid use, or surgical planning? This lack of clinical metadata renders the volumetric findings speculative at best.
The study uses 25 patients, yet compares 135 distinct brain structures, creating an immense multiple comparisons problem. Bonferroni or FDR correction? Not discussed. This opens the door to false positives and spurious correlations, undermining the credibility of the statistical claims.
Vol2Brain, HIPS, and Ceres are invoked as if their combined use inherently validates the pipeline. But multi-software approaches do not substitute for clinical rigor or biological plausibility. Their use appears more ornamental than scientific, producing beautifully color-coded brain maps detached from meaningful interpretation.
There is no mention of cognitive status, anti-epileptic drugs, corticosteroid usage, or duration of disease — all of which can affect brain volume. Comparing a neurologically symptomatic AVM group with healthy controls without adjusting for these is intellectually dishonest.
The authors allude to “mass effect”, “neuroplasticity”, and “remote volume change”, but never commit to a mechanistic model. The result is a soup of vague neuroanatomical inferences built on shaky anatomical correlation.
The conclusion leaps from a narrow MRI study into speculative clinical territory: “Understanding these volumetric changes can aid in explaining patient symptoms.” Really? Which symptoms? Were any clinical correlations measured? This is hypothesis-generation disguised as practice-changing insight.
Multiple keyword redundancies (“hipocampo”, “hippocampus”, “volumen cerebral”) and translation inconsistencies reflect a lack of editorial care. The title also oversells the scope of the findings.
This paper is a textbook example of how software-enabled volumetric analysis can produce data-rich but insight-poor conclusions. Its methodological fragility, small sample size, and exaggerated claims about remote structural changes reduce it to a cautionary tale in neuroimaging interpretation.
Buzzword Inflation Index: 9/10
Scientific Merit: 3/10
Clinical Impact: 1/10
Final Assessment: Technically elaborate, clinically irrelevant. Another case of *when segmentation pipelines run faster than critical thinking*.