Good something.

We are presented with a case of a 13-year-old male with a 2-month history of mass on the right face
associated with fever, responding to antibiotics. A 1-month history of sudden onset left hemiparesis, with associated dizziness,
dysphagia and cough. On the day of admission patient was sent to the hospital due to altered mental status, left sided
weakness, left sided ataxia and vertical nystagmus. The case did not mention of …..

Beginning with our cc of altered mental status with concomitant focal neurological deficits as our pivot point, we can approach
this case primarily by levelizing, lateralizing and localizing our possible etiology of our patient’s demise. First we levelize by
differentiating symptoms whether it is of central or peripheral origin. Peripheral symptoms usually presents as a localized
deficit, usually involving the following -----------------. Due to the involvement of the cranial nerves and associated weakness of
one side of the body, this will point us towards a more centrally located lesion. We can classify these lesions under
supratentorial or infratentorial regions. Supratentorial lesions involves the cortex and subcortical structures usually presenting
with seizures, language disorders, behavioral changes and the like, while infratentorial lesions presents with gait disturbances,
movement coordination, ataxia, cranial nerve involvement and long tract signs, thus leading us more to a infratentorial lesion.
Left sided symptoms seen in our patients points to a right sided lesion as tract decussate below the pyramids of the medulla,
hence the contralateral location. And finally to localize our lesion, infratentorial structures include the brainstem or
cerebellum, which presents as the following (SHOW TABLE OF SYMPTOMS AND HIGHLIGHT SEEN IN THE PATIENTS), hence we
are considering the involvement of both the cerebellum and brainstem.

And now at this point in time we must ask ourselves the etiology of the lesion. Lesions may be of different etiologies including
VITAMIN CD. Since there is no history of prior trauma, this category can be eliminated. Most autoimmune diseases presenting
with weakness commonly manifest with bilateral symptoms, making it an unlikely diagnosis. Metabolic causes such as
nutritional deficiency, electrolyte problems, toxicities and drug intoxication also present with bilateral symptoms, together with
a lack of history from these sources, this etiology may be ruled out. Iatrogenic causes can be ruled out due to lack of previous
procedures done to the patient while degenerative diseases can also be ruled out due to patient demographic not compatible
with common degenerative diseases such parkinson’s, alzhemers and the like.

Now we are left with the following categories, vascular, infectious, neoplastic and congenital. Starting with vascular causes, a
differential would be stroke in the young (ade’s part). Considerations under the infectious category include bacterial and
parasite in origin. Under bacterial we can consider (to find the most common bacterial cause) meningitis and tuberculoma.

Tuberculous meningitis occurs in about 0.3% of untreated tuberculosis infection in children. The incidence of central nervous
system TB meningitis is related to the prevalence of TB in the community, and it is still the most common type of chronic CNS
infection in developing countries. The clinical progression of tuberculous meningitis may be rapid or gradual, and tends to occur
more rapidly in the pediatric age group. Non specific signs such as fever, and behavioral changes typically progress over several
weeks in TB meningitis. TB meninigitis arises from bacterial seeding of the meninges and subpial regions of the brain with
formation of tubercles, followed by the rupture and discharge of tubercle bacilli into the subarachnoid space. This leads to an
infection of the meninges, cortex, and brainstem; as well as blockage of flow of CSF at the level of the basilar cisterns, leading to
a communicating hydrocephalus. Hemiparesis, cranial nerve palsies, and other focal neurologic signs could also be strongly
correlated to mass effect caused by the development of hydrocephalus affecting the brainstem area.

Radiologically, in CT imaging, TB meningitis manifests as a triad of hydrocephalus, basal ganglia/thalamic infarcts, and basal
enhancement, but in contrast to our case, there was no noted infarct in the CT scan imaging. Although rare, true tuberculous
abscess resulting from TB meninigitis could present in the cerebellar area, but CT scan wise, most tuberculous abscess are
described as ill-defined hyperintense lesions with subsequent ring enhancement on post contrast study, in contrast to our case
which revealed a hypodense focus on the vermis. Thus, TB meningitis can be ruled out.

Tuberculomas are tumor-like masses of tuberculous granulation tissue, most often multiple but also occurring singly, that form
in the parenchyma of the brain. The larger ones may produce symptoms of a space-occupying lesion and periventricular ones
may cause obstructive hydrocephalus.In our case, this could explain the presence of constitutional symptoms such as fever and
altered sensorium, similar to TB meningitis.
 Also, epidemiologically wise, cerebellar tuberculomas are the most frequent intracranial tumors in children in tropical
countries. We could strongly attribute this to the development of cerebellar symptoms such as ataxia and vertical nystagmus.

Radiologically, characteristic CT finding is a nodular enhancing lesion with a central hypodense region. In the early stage,
however, lesions may be isodense, often with edema out of proportion to the mass effect along with little encapsulation. Late
in their development, well-encapsulated tuberculomas appear as isodense or hyperdense lesions with peripheral ring
enhancement. With these, tuberculoma cannot be ruled out.

(Eunice partwhile under the parasitic category considerations include cerebral hydatid cyst and neurocystcercosis (Raymond
part). Under the congenital category, consideration points to a AV malformation rather than other diseases since symptoms of
av malformation maybe absent at birth but may present later at life (READ MORE BITCH).

Any tumor occupying the posterior fossa would present with almost similar clinical features. Among them, we consider the top
causes of pediatric posterior fossa neoplasms, which include medulloblastoma, pilocytic astrocytoma, ependymoma and
brainstem glioma.

Medulloblastoma is a malignant embryonal tumor which occurs predominantly in children and exclusively in the cerebellum
usually midline. Children with medulloblastomas often present clinically with a relatively rapid onset of symptoms, usually over
the course of weeks or a few months with symptoms presenting as truncal ataxia, symptoms of hydrocephalus, and
papilledema.

Another etiology is pilocytic astrocytoma, being the most common pediatric cerebellar neoplasm and represents 1/3 of all
pediatric posterior fossa tumors. 50 percent of are seen within the cerebellar hemisphere but can also be seen on the optic
pathways and hypothalamus, with symptoms presenting as headache, nausea, vomiting, gait disturbance and visual
disturbances.

Ependymomas are tumors that most often arise next to the ependyma lined ventricular system, which commonly present at
the first two decades of life and typically occur near the fourth ventricle. They are the third most frequent brain tumor in the
pediatric population and present clinically as symptoms related to hydrocephalus.

And finally, brainstem gliomas are tumors which encompass 20% of all CNS tumors in the pediatric population. The most
common subtype, diffuse intrinsic pontine gliomas, accounts for over 80% of all brainstem gliomas with a mean age of 7-9
years. They usually present with aggressive course and poor prognosis.

2) Infectious to rule out stroke in the young.

To further investigate and narrow down our diagnosis, ancillary procedures were requested and are as follows.

An earlier CT scan of the brain and paranasal sinus reveal an enlarged pons with no definite enhancing mass with associated
hydrocephalus. There was also a non-enhancing mass found in the right maxillary sinus as well as mucosal thickening
in the sphenoid sinus.

Upon admission patient was subjected again to topography with results revealing fairly defined hypodense mass in the vermis
with subsequent hydrocephalus and with a hypodense focus in the pontine region. Partial opacification was now
noted in the right maxillary sinus in contrast to earlier findings of a non-enhancing mass on the same area.

Chest Xrays also reveal presence of pneumonia

Blood work-ups reveal an elevated WBC counts with elevated neutrophils and eosinophils on both instances. Blood chemistry
are essentially normal. (LOOK SOURCE OF EOSINOPHILIA IE SINUSTIS ALLERGIES CHUCHU)

RULE IN RULE OUT TABLES

FINAL DIAGNOSIS

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