The presentation of the signs and symptoms of astrocytoma depends heavily on the tumor location and the extent of growth. Any neurological symptomatology detected in the early phase of the disease must prompt physicians to subject patients to further diagnostic tests and imaging studies to guide them with the management and prognosticate outlook respectively. The following presentations are seen in the early stages of the disease:
- Visual disturbances when the optic nerve is impinged.
- Headaches due to an increase in intracranial pressure.
- Altered mental state due to the metabolic imbalance within the brain matter.
- Cognitive impairment due to the cerebral damage.
- Seizures due to metabolic imbalance and increased intracranial pressure.
- Motor paralysis due to impaired spinal and brainstem function.
- Ataxia is caused by cerebellar damage by the enlarging tumor.
The following laboratory workup and imaging modalities are implored in the diagnosis and management of astrocytoma tumors:
- Serum electrolytes
- Complete blood count (CBC)
- Prothrombin time (PT)
- Activated partial thromboplastin time (APTT)
- Computed tomography (CT scan)
- Magnetic resonance imaging (MRI)
The role of surgery in the treatment of astrocytoma is two folds:
- To remove or debulk the astrocytoma tumor to relieve compression signs, and
- To gather samples for histologic diagnosis, guide adjuvant therapy and prognosticate clinical course of the disease .
Palliative neurosurgery by draining the excess cerebrospinal fluid to the ventricles or by doing a ventriculo-peritoneal shunt may decompress the brain. A complete resection of the astrocytoma tumor offers the best prognosis for patients by increasing the mean survival rate .
In low grade astrocytoma, a subtotal resection of the tumor mass may be indicated conferring a better survival rate . For patients presenting with seizures, the use of phenytoin and carbamazepine may be imperative to prevent further complications.
The relative prognosis in astrocytoma tumor depends on the grading of the tumor. Low grade tumor may have uncomplicated neurologic deficits may live in up to 10 years compared to high grade astrocytoma where survival rate only reaches 2 years. The size of the tumor correlates directly with increase in intracerebral pressure and the morbidity of the patients. The morbidity rate and mortality rate improves significantly with the early diagnosis and the prompt removal of the tumor.
The following complications are associated with patients diagnosed with astrocytoma:
These primary brain tumor starts out as a normal cells that acquire mutations in their DNA which allow them to divide continuously in an increasing rate and wouldn’t conclude in cell death. The amassing of these cells results in a primary brain tumor.
The yearly incidence of astrocytoma tumors in the United States and internationally is uniformly observed at 54 cases per million population. In pilocytic astrocytoma, the mean survival duration is 10 years while those with low grade diffuse astrocytoma may survive beyond 5 years .
There are no racial predilection on the prevalence rate of astrocytoma. There is a slight male predominance over female at a ratio of 1.18:1 for low grade astrocytoma. The prevalence of pilocytic astrocytoma peaks on the second decade of life while those for low grade astrocytoma peaks at the third to fourth decade of life.
The primary pathophysiology in astrocytoma is associated to its inherent capacity to grow incessantly and cause compression, invasive and destructive signs in the brain parenchyma.
Compressive signs are hallmarked by the impingement of the arterio-venous blood supply of the brain parenchyma causing eminent tissue hypoxia. The rapid growth of the tumor competes with the limited supply of nutrients in the brain matter and starves the normal cells. Astrocytoma releases metabolic end products (free radicals) and recruits cellular mediators like cytokines that disrupts normal parenchymal functions.
The space occupying effect of the tumor causes an increase in intracerebral pressure and an increase in cerebrospinal fluid which causes other compression effects to other contiguous structures of the brain. Local mass compression causes weakness, paralysis, sensory deficits and cranial nerve palsies which allows for the localization of the lesion by means of an extensive neurologic examination .
In cases of anaplastic astrocytoma, the occurrence of clinical symptoms from the time of diagnosis is usually intermediate to low grade astrocytoma and glioblastoma with lower incidence of seizures . They usually present with depressed mental state, headaches, and focal neurologic symptoms.
Primary brain tumors like astrocytomas are not preventable; thus, no modifiable activities may be implored to prevent its occurrence. The early identification of the disease by its early sign and symptoms is paramount in the success of it treatment. The prompt resection of the tumor may offer the best outcome and prevent long term complications. Frequent neurologic follow ups may be required especially in low grade astrocytomas because of its high rate of recurrence .
Astrocytomas are primary brain tumors that develops from the brain parenchyma. Astrocytoma are brain neoplasms that are derived from the immortalized actrocyte components of the neural tissues . They represent the second most common primary brain tumor . There at least two classes of astrocytoma: those with narrow zone of infiltrations and those with diffuse zone of infiltration.
Astrocytomas may arise from any part of the central nervous system (CNS) with preference on the cerebral hemisphere. The clinical presentation is usually evident during adulthood and may remain asymptomatic during childhood. All astrocytoma tumors has a propensity to advance into higher grades. A World Health Organization (WHO) grading scheme is adapted in the classification of astrocytoma in reference to the presence of nuclear atypia, degree of mitotic activity, vascular proliferation, cellularity and amount of necrosis .
Astrocyte and glial cell DNA mutations cause the development of these tumors.
Cranial computed tomography (CT) scan and magnetic resonance imaging (MRI) are commonly used to diagnose the disroder.
Treatment and follow-up
Primary resection of the tumor through craniotomy and adjuvant therapy is usually the treatment option of choice.
- Greenberg MS. Astrocytoma. In: Handbook of Neurosurgery. Vol 1. 4th ed. Lakeland, Fla: Greenberg Graphics Inc; 1997:244-256.
- Helseth A, Mørk SJ. Neoplasms of the central nervous system in Norway. III. Epidemiological characteristics of intracranial gliomas according to histology. APMIS. Jun 1989; 97(6):547-55.
- Kleihues P, Burger PC, Scheithauer BW. The new WHO classification of brain tumours. Brain Pathol. Jul 1993; 3(3):255-68.
- Kleihues P, Davis RL, Ohgaki H. Low-grade diffuse astrocytoma. In: Kleihues P, Cavenee WK, eds. Pathology and Genetics: Tumours of the Nervous System. Lyon, France: International Agency for Cancer Research; 1997:10-14.
- Kesari S. Understanding glioblastoma tumor biology: the potential to improve current diagnosis and treatments. Semin Oncol. Dec 2011; 38 Suppl 4:S2-10.
- Davis RL, Kleihues P, Burger PC. Anaplastic Astrocytoma. In: Kleihues P, Cavenee WK, eds. Pathology and Genetics: Tumours of the Nervous System. Lyon, France: International Agency for Cancer Research; 1997:14-15.
- Laws ER Jr, Taylor WF, Clifton MB, Okazaki H. Neurosurgical management of low-grade astrocytoma of the cerebral hemispheres. J Neurosurg. Oct 1984; 61(4):665-73.
- Lacroix M, Abi-Said D, Fourney DR, Gokaslan ZL, Shi W, DeMonte F, et al. A multivariate analysis of 416 patients with glioblastoma multiforme: prognosis, extent of resection, and survival. J Neurosurg. Aug 2001; 95(2):190-8.
- Duffau H. A new philosophy in surgery for diffuse low-grade glioma (DLGG): oncological and functional outcomes. Neurochirurgie. Feb 2013; 59(1):2-8.
- Chaichana KL, McGirt MJ, Niranjan A, Olivi A, Burger PC, Quinones-Hinojosa A. Prognostic significance of contrast-enhancing low-grade gliomas in adults and a review of the literature. Neurol Res. Nov 2009; 31(9):931-9.