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Be a part of International Conference on Neurosurgery

Scientific Program


December 08-09, 2021 at 10:00 AM DXB 
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Dubai, UAE

Keynote Session:

Oral Session 1:

Meetings International - NEUROSURGERY 2021 Conference Keynote Speaker Dr Habiba Abdullahi  photo

Dr Habiba Abdullahi

Medical Student at Near East University School of Medicine, Cyprus



Dr Habiba Abdullahi is a 4th year medical student at Near East University School of Medicine, Cyprus. She is intrested towards the research and developments in Pediatric Neurosurgery.


A stroke occurs when the blood supply to a part of the brain is disrupted or reduced, preventing brain tissue from getting oxygen and nutrients which causes brain cells to die in minutes and according to the part of brain affected, loss of function occurs. In more scientific terms, it is a clinical, radiological, or pathological evidence of ischemia or hemorrhage, involving a defined cerebral vascular territory(1). It is the leading cause of disability in the USA and a major cause of mortality worldwide(2).

Strokes can be categorized as ischemic (inadequate blood supply to the brain) or hemorrhagic (bleeding into the brain); which is the less common type. Although rare, pediatric stroke is the leading cause of morbidity and mortality in children. This is due to delayed diagnosis which is because of delay in seeking medical attention. Stroke, in pediatric patients is defined by the same criteria as adults, however in these patients, unlike adults, the acute presentation is missed. Population-based studies of arterial ischemic stroke(AIS) in children(age 29 days-18 years) estimate an annual incidence of 2.4 per 100,000 persons with a case fatality approaching 4(3),(4). Even amongst the survivors, there are very high chances of long-term disabilities. Over 50% of the survivors have persistent neurologic, cognitive, or psychiatric problems. The management of stroke in pediatric population is also highly challenging due to lack of literature, basing treatment solely on following adult stroke management.

There are different ways of classifying stroke in pediatric patients. By age: from 28 weeks of gestation to 28 postnatal days of life is generally called PERINATAL STROKE which present with focal seizures and sensorimotor deficits as the child ages(5),(6).Some authors have expanded this interval to begin from 20 weeks of gestation because lesions even before the 28th week of gestation has been documented(7). Stroke occurring after 28days of life to 18 years is CHILDHOOD STROKE which presents with acute focal neurological deficits e.g. hemiparesis(5), (6).Perinatal stroke occurs in 1 in 2300 live births while childhood stroke occurs in 2-3 per 100,000(8), (9). Acute perinatal stroke presents shortly after onset with focal seizures and encephalopathy. Presumed perinatal stroke are chronic infarcts, diagnosed in a delayed manner that are presumed to have occurred in the perinatal period(6). These patients exhibit no symptoms in the perinatal period, thus are not detected until a hemiparesis occurs later on within the first year(5). Infants with this present with pathologic early handedness or seizures, which subsequently leads to brain imaging and diagnosis(10).

Ischemic stroke constitutes arterial ischemic stroke (AIS) and venous thrombosis caused by cerebral sinovenous thrombosis(CSVT) and cortical vein thrombosis(6). About 80% of the lesions in perinatal stroke are ischemic(arterial ischemic stroke) and the rest, are due to hemorrhage or cerebral sinovenous thrombosis(CSVT)(11). The ratio of ischemic stroke is significantly higher in newborns, almost 6 times more than in older children(12).

Newborns with AIS typically present with seizures, specifically focal motor seizures involving only one extremity, and this is seen rarely in older children(13)(14). The left cerebral hemisphere is affected in 80% of neonates with unilateral infarctions(14).

In the adult patients, stroke is generally due to atherosclerotic risk factors like hypertension, diabetes mellitus, dyslipidemia, obesity etc. In children and adolescence, atherosclerosis is generally not a causative factor of stroke, but it’s evident that the atherosclerotic process that ultimately causes stroke in adults begins from childhood and that dyslipidemia is more common in children with ischemic stroke than other children(15). Main risk factors in pediatric stroke include both maternal and neonatal factors. It is speculated that normal levels of coagulation factors in mothers and low levels of factors in the infant just before and after the time of delivery contributes to increased stroke risk in neonates(7).Neonates with Acute ischemic stroke sometimes have inherited thrombophilia(16). Other risk factors correlated with neonatal acute ischemic stroke are cardiac lesions, coagulation disorders, infection, trauma and asphyxia(7), (9)(17). Recently, COL4A1 mutations which is a subunit of type IV collagen that plays a role in angiogenesis has been recently linked to intrauterine stroke and porencephaly(18), (19).  Some maternal factors, e.g., oligohydramnios, premature rupture of membranes, history of infertility, emergency cesarean section, pre-eclampsia may be associated with perinatal acute ischemic stroke (AIS). Even though all the risk factors mentioned have been proven to increase the chances of AIS, no single cause has been isolated(20), (9).

The most important thing needed for a full recovery in pediatric stroke is adequate management and prevention. The standard of care is certain interventions to obtain physical, occupational, speech and language therapy and neuropsychological interventions(5). Prevention can be done by targeting the risk factors. Therapy, rehabilitation, and recovery is a bit complex in pediatric patients because some deficits are not obvious till a long time after the stroke has occurred. There is little known about the acute treatment and recovery techniques specific to pediatric patients. For management, there is supportive care which constitutes optimization of oxygenation, control of seizures, and the correction of dehydration and anemia(21). Antiplatelet therapy is considered only in neonates with high risk of recurrent AIS due to thrombophilia or congenital heart disease(22), (23). Thrombolysis has been approved for use only in children 18years and older and not considered in neonates, although, there has been recent research that aims to establish the safety and feasibility of thrombolysis using tissue plasminogen activator(tpA) intravenously and intraarterially for AIS in younger children(ages 2-17)(6), (24), . Endovascular procedures e.g. mechanical thrombectomy have been approved for in older children with occlusion but these are not used in neonates because of the small size of their arteries(21), (25).Most of the children with AIS experience residual neurological deficits including cerebral palsy, cognitive speech impairment, and epilepsy(26).

There have been promising therapies to aid in the recovery of pediatric stroke patients. Such therapies include Constraint induced movement therapy (CIMT) to improve motor outcomes. Use of noninvasive brain stimulation to aid in the prognosis or modify outcomes of children after pediatric stroke is beginning to look promising as an adjunctive treatment to promote recovery(5). Stem-cell based treatments have been explored but there is less evidence of its success in pediatric patients(5), (27).

Outcomes after pediatric stroke are good, but moderate to severe neurological impairments are still seen especially between 28 days and 1 year because these are vulnerable ages(28), (29), (30),(31). Another research showed that most of the recovery occurs 2-3 months after stroke, and quality of functional recovery was better in pediatric than the adult population, and it’s believed that the window for recovery is longer for children(32), (33). This could be due to the ‘Kennard principle’ by Margaret A. Kennard which is that younger brains naturally recover better than older brains(34).

Generally, recovery of pediatric stroke depends on age/stage of development, presentation, speed of diagnosis.


Oral Session 2:

  • BROCA aphasia complicating acute malarial encephalitis, Neuroadapted Therapeutic Approach: Place of Citicholine and Neuroregulators in prevention, reduction of sequelae neurological and morbidity and mortality.
Meetings International - NEUROSURGERY 2021 Conference Keynote Speaker Dr. Lamirez Diasivi Nzuzi photo

Dr. Lamirez Diasivi Nzuzi

Mont-Amba University Hospital Center (CHMA), University of Kinshasa

Title: NEWS ON NEUROPALARIA: BROCA's aphasia complicating encephalitis acute malaria, Approach Neuroadapted Therapeutics: Place of Citicholine and Neuroregulators in prevention, reduction of sequelae neurological and morbidity and mortality.


Dr. Lamirez Diasivi Nzuzi is working for the department of neurosurgery at Mont-Amba University Hospital Center (CHMA), University of Kinshasa.




Cerebral malaria, acute malarial encephalitis due to Plasmodium falciparum: is an acute brain injury whose outcome may be fatal can lead to polymorphic neurological sequelae: hemiplegia / hemiparesis, speech disorders (motor aphasia de Broca, Sensory aphasia of Wernicke), behavioral disturbances, cognitive impairment, blindness, secondary epilepsy. In Africa Sub-Saharan, and more particularly in the DRC, Neuropalaria, knows a high frequency of neurological lesions with a very high lethality and the seriousness of their repercussions on the fate of the children who are victims of it. The neuropathological severity of acute malarial cerebral aggression is correlated with the high parasite density, with the phenomena of sequestration and cytoadherence, the inflammatory process, the presence of the factors of bad prognosis or ACSOS, the diagnostic and therapeutic delay; and the antimalarials, do not modify the evolutionary process of neurological lesions and those of sequelae. An approach Neuroadapted therapy (Citicholine and neuroregulators) introduced in our patients, from the acute phase (from D0: in first 24 hours / first 6 hours +++ to 7 days), until the stabilization phase (D0- 30 days), allowed us to: Improve perfusion of the areas of ischemic brain suffering, regulation of cerebral metabolism (aerobic glycolysis +++) and reduction of cerebral edema (vasogenic, cytotoxic +++); delay the evolution of the destruction of the neuronal membrane and neuronal degeneration; limit and block ischemic cascades leading to neuronal necrosis; Improve the prognosis and dramatic rapid recovery, speech recovery and significant reduction in other neurological sequelae, but also death-mortality.
To date, acute malarial encephalitis should be considered in mind as a normotensive ischemic stroke. post-infectious, until proven guilty, in the light of the neuroanatomo-clinical correlation, of the neurophysio- pathologies induced in acute and secondary cerebral aggression.
Management of acute malarial encephalitis and its acute complications, and to propose a Neuroadapted therapeutic approach, by demonstrating the action of Citicholine and neuroregulators on Broca's area.
A serial study of cases admitted to the Emergency and Neuropediatrics Department for acute malarial encephalitis complicated by aphasia de Broca and other neurological sequelae.
In the absence of certain medical files available and in the insufficiency of clinical and para-clinical data found in certain records, of the 30 patients registered for acute malarial encephalitis complicated by neurological deficits during the period of March 2021, we describe that two cases of Broca's Aphasia on Acute Malarial Encephalitis in two patients born and residing in DRC, Kinshasa. The first case; a 9-year-old male child admitted to the neuropediatric emergency room for tonic-clonic seizures and headaches, in his antecedents, no notion of previous seizure episode, no convulsors and epileptics in the family. Treatment received elsewhere, Quinine, Ciprofloxacin and Diazepam; In whom we note mainly at physical examination, Heart rate at 140 bpm, Respiratory rate at 40 cpm, Temperature at 38 ° C, Coma with convulsions
Tonic-clinical, febrile on palpation, colored eyelid conjunctivae and anicteric bulbar conjunctiva, an abdomen not bloated, sensitive to medium ureteral points and without organomegaly, Deep coma, Soft neck and no signs of neuro-irritations meningeal, isocoric and reflective pupils. On paraclinical examination, Hb at 12 g / l, occasional glycemia at 109 mg / dl, GE: Tropho +++, GB: 16000 elt and FL: N60% L40%; Widal (TH: 1/160, TO: 1/160), Blood ionogram, CT-brain scan and emergency EEG not performed, a treatment was initiated: made of injectable Artesunate (H0-H72), Oritaxim, Amikacin, Ciprofloxacin, a maintenance infusion :( SG5% + electrolytes + Nootropyl + Azantac) and feeding by gavage. The evolution would be marked on D5-D7 by an awakening initiated with Brocas motor aphasia, right hemiparesis, CT scan of the brain, performed: Left frontal hypodensity zone. Under Citicholine(Somazina) and Neuroregulators (Gamalate B6, Surmenalite), resumption of language 24 hours later, with end of tremors (impairment of central gray nuclei) under Artane ½ tablet for 7 days with a good spectacular development. File close and exit authorized with Trausan, Surmenalite and Gamalate B6 for 1 month; an appointment in 1 month with a cerebral CT-scan control.
The second case; she is a 27-year-old patient, admitted for temporo-spatial disorientation and headache. contributory, in whom the clinical examination notes a BP: 158/87 mm Hg, HR: 112bpm, FR: 24 cpm, patient with temporal disorientation spatial, EG altered by suffering mine, Colored eyelid conjunctiva and bulbar anicteric, on normal gynecological examination, on neurological examination; flexible neck and no signs of neuro-meningeal irritation, isocoric and reflective pupils. At the exam paraclinical; GE: Tropho +; incidental blood sugar: 112 mg / dl, Hb: 12 g / l, ESR: 60mm / H, GB: 12200elt, FLN62% L38%, Urinary sed (GB: 5-10 / elt, EC: 5-10 / elt), treatment with Artesunate, promethazine, ceftrin plus. The evolution was marked by a motor aphasia of Broca, a few hours after admission, a cerebral CT scan was urgently requested, not carried out given the financial situation patient, and she was on citicholine (Somazina) as a continuous infusion with antioxidants (VIT C, VIT E) in emergency, neurosedation with phenobarbital. On day 1 of hospitalization, i.e. 24 hours of hospitalization later, we observed the resumption of speech with temporo-spatial orientation, and vital signs in physiological norms. File close and exit authorized with Somazina tablet, Gamalate B6, Overmenalitis for 1 month.
Before any case of acute malarial encephalitis (cerebral malaria), it is of interest to add the neuroregulatory therapeutic regimen; improving the prognosis (rapid recovery), preventing the occurrence of neurological complications often irreversible and reduced morbidity and mortality. And Antimalarials, do not modify the evolutionary process of destruction neuronal and neurological sequelae.


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