The limits of neuroplasticity - or are there any?

Right now, neuroplasticity is not repeatable on demand. 

When your incompetent? doctor uses this word ask then to EXPLAIN EXACTLY what needs to happen for a neuron to drop a current task and take on a neighbors! 

NO explanation; PURE FUCKING INCOMPETENCE! Not knowing that makes neuroplasticity non repeatable on demand!

 The limits of neuroplasticity - or are there any?

Katerina Poprelka1  · Maria Stefanatou1 · Stylianos Gatzonis1 Received: 9 May 2026 / Accepted: 26 September 2026 © Fondazione Società Italiana di Neurologia 2026 

To the Editor, Cases demonstrating discordance between marked structural brain abnormalities and preserved clinical function are rare but informative. We report such a case in a 52-year old woman, highlighting the limits and resilience of neuro plastic adaptation. The patient presented to the outpatient neurology clinic following two witnessed generalized tonic-clonic seizures, both associated with a postictal phase of impaired awareness, drowsiness, and confusion, with gradual recovery over several minutes. On examination, she was alert and oriented, with no focal neurological deficits. However, deep tendon reflexes were brisk throughout, and plantar responses were indifferent bilaterally. Her past medical history was notable for childhood men ingitis, the exact etiology of which was not documented, and longstanding macrocephaly. No prior neurosurgical intervention has been reported. Despite these early neuro logical factors, she achieved normal developmental mile stones, completed secondary education, and maintained consistent employment, indicating a high level of functional adaptation. She had no history of epilepsy until the age of 43, when she began experiencing focal seizures characterized by impaired awareness, automatisms, and behavioral arrest, consistent with focal impaired awareness seizures. These were managed with lacosamide at a dose of 150 mg twice daily. In 2023, she experienced an episode of status epilepticus, precipitated by poor medication adherence. Fol lowing this, brivaracetam was added to her treatment regi men, resulting in improved seizure control. Neuroimaging revealed striking abnormalities. A CT scan demonstrated marked enlargement of the lateral and third ventricles, consistent with severe ventriculomegaly, along with significant thinning of the cortical mantle. Brain 1 Katerina Poprelka katerinapop@med.uoa.gr First Department of Neurosurgery, Evangelismos Hospital, National & Kapodistrian University of Athens, 45-47 Ipsilantou Str., Athens 10676, Greece MRI (Fig. 1) provided further detail, showing diffuse cere bral atrophy, most prominently involving the corpus cal losum, which appeared significantly thinned. Additionally, an empty sella turcica was noted. Electroencephalogra phy showed generalized slowing with predominant theta activity, intermittent epileptiform discharges, and bilateral temporo-occipital slowing, more prominent over the left hemisphere. We believe that the observed ventricular enlargement most likely reflects a long-standing developmental or post inflammatory process, rather than active hydrocephalus. The available clinical and imaging data do not allow a clear distinction between chronic post-infectious hydrocephalus, arrested hydrocephalus, and long-standing overt ventriculo megaly in adults (LOVA). The degree of ventricular enlarge ment is disproportionate to the observed cortical atrophy, making hydrocephalus ex vacuo less likely. We therefore favor a multifactorial explanation involving chronic ventric ulomegaly with secondary cerebral atrophy, while acknowl edging the inherent diagnostic uncertainty. A comprehensive neuropsychological assessment was conducted to evaluate cognitive functions in greater depth. Mild executive dysfunction was observed, particularly affecting cognitive flexibility, planning, and processing speed, as evidenced by reduced performance on Stroop Neuropsychological Screening Test, Trail Making Test Part B, and Digit Symbol Coding. Memory performance was dis proportionately affected, with severe impairments in verbal and visual learning and delayed recall on the Rey Auditory Verbal Learning Test and the Rey-Osterrieth Complex Fig ure Test, suggesting deficits across encoding, consolidation, and retrieval processes. Increased susceptibility to interfer ence was also observed. The non-modality-specific pattern, affecting both verbal and visual memory, points to dysfunc tion within distributed memory networks rather than a focal deficit. Despite these objective deficits, the patient did not report significant subjective cognitive complaints in daily life. However, cognitive fatigue was observed during test ing, which may have contributed to reduced performance and suggests limited cognitive reserve under sustained  demand. Importantly, there was no evidence of coexisting mood or anxiety disorders that could otherwise explain or exacerbate cognitive findings. The prevalence of hydrocephalus in the adult population is estimated at roughly 1 per 10,000, with aqueductal steno sis accounting for approximately 10% of cases [1]. Additional common etiologies include congenital abnormalities, infec tious processes, head trauma, and space-occupying obstructive lesions. Among these etiologies, long-standing hydrocepha lus, including cases secondary to early-life insults such as infection, is of particular interest, as it may be associated with severe anatomical distortion yet relatively preserved clini cal function. This case demonstrates a marked dissociation between extensive structural brain abnormalities and func tional outcome. Although the degree of ventriculomegaly, cor tical thinning, and diffuse atrophy would typically be expected to result in significant neurological and cognitive impairment, the most striking feature in this patient is the preservation of functional independence despite objectively significant neu ropsychological deficits, including severe memory impair ment and mild executive dysfunction. Notwithstanding these findings, she maintained autonomy in everyday activities for decades, underscoring a complex and non-linear relationship between cognitive impairment and real-world functioning. Similar cases have been described in the literature, particularly in individuals with long-standing or congenital hydrocepha lus, in whom profound anatomical distortion is accompanied by relatively mild clinical manifestations [2, 3]. A 44-year-old man with a history of childhood hydro cephalus and shunt placement demonstrated severe ventricu lomegaly and a markedly thin cortical mantle, accompanied by low-average intellectual functioning; nevertheless, he maintained functional independence and relatively stable neurological status over time, with cognitive deficits that appeared chronic rather than progressive [2]. Similarly, in a (C) Sagittal and coronal views illustrating the marked expansion of the ventricular system and compression of the brain parenchyma 72-year-old woman with overt ventriculomegaly, preserved independence and normal cognitive screening were reported despite severe structural abnormalities, with seizures emerg ing late in life in the context of otherwise minimal neurolog ical impairment [3]. Compared with these cases, the present patient shares the characteristic dissociation between severe structural brain changes and preserved daily functioning; however, she is distinguished by more pronounced memory impairment on formal neuropsychological testing despite long-term independence. These observations may be considered within the frame work of developmental plasticity, whereby cognitive func tions developing in the context of early neurodevelopmental abnormalities may adapt to an atypical neural substrate. In this context, adaptation is more appropriately conceptual ized as the development of cognitive functions within exist ing structural constraints rather than as “reorganization” of previously established networks. Such developmental adaptation may partly account for the preservation of func tional independence despite severe structural abnormalities, although the mechanisms underlying this dissociation can not be established from the present case. The presence of significant memory impairment and milder executive dys function, together with the later emergence of epilepsy, nev ertheless suggests that this adaptation may be incomplete and may not fully protect against cognitive and neurological vulnerability. Cognitive reserve may also have contributed to the relatively preserved everyday functioning; however, available proxies are limited to educational attainment and sustained employment, precluding stronger conclusions regarding its role. Age-related changes, increasing network inefficiency, and reduced cognitive reserve have been pro posed as factors that may reveal previously compensated vulnerabilities over time; however, their contribution in the present case remains speculative 

In summary, this case highlights that functional outcome in chronic structural brain disease is not determined solely by anatomical integrity. Instead, the marked dissociation between structural abnormalities and everyday functioning may reflect the influence of developmental adaptation and individual differences in cognitive reserve, although their respective contributions cannot be established in this case. While the brain demonstrates remarkable adaptability in the context of longstanding structural abnormalities, cognitive deficits and neurological complications may still emerge, underscoring the importance of comprehensive evaluation and long-term follow-up. 

Author Contribution Credit authorship contribution statement Kateri na Poprelka: Conceptualization, Investigation, Formal Analysis, Writ ing Original Draft. Maria Stefanatou: Validation, Writing- Review & Editing. Stylianos Gatzonis: Supervision, Writing- Review & Editing. Funding No funding was received to assist with the preparation of this manuscript. Declarations Ethics approval The authors have obtained patient consent. Competing interest The authors have no competing interests to de clare that are relevant to the content of this article. References 1. 2. 3. Oi S, Shimoda M, Shibata M, Honda Y, Togo K, Shinoda M, Tsu gane R, Sato O (2000) Pathophysiology of long-standing overt ventriculomegaly in adults. J Neurosurg 92:933–940. h t t p s : / / d o i . o r g / 1 0 . 3 1 7 1 / j n s . 2 0 0 0 . 9 2 . 6 . 0 9 3 3 Feuillet L, Dufour H, Pelletier J (2007) Brain of a white-collar worker. Lancet 370:262. h t t p s : / / d o i . o r g / 1 0 . 1 0 1 6 / S 0 1 4 0 - 6 7 3 6 ( 0 7 ) 6 1 1 2 7 - 1 Persad AR, Bass V, Meguro K (2021) Asymptomatic hydrocepha lus. CMAJ 193:E480. https: //d oi. or g/10 .150 3/cmaj.200889 Publisher’s Note Springer Nature remains neutral with regard to juris dictional claims in published maps and institutional affiliations