Meningitis typically occurs through two routes of inoculation:

We have the Hematogenous seeding and Direct contiguous spread.

Bacteria are transported across epithelial cells in membrane-bound vacuoles to the intravascular
space or invade the intravascular space by creating separations in the apical tight junctions of
columnar epithelial cells.
Now, once in the bloodstream, bacteria are able to avoid phagocytosis by neutrophils and classic
complement-mediated bactericidal activity because of the presence of a polysaccharide capsule.
Bloodborne bacteria can reach the intraventricular choroid plexus, directly infect choroid plexus
epithelial cells, and gain access to the CSF. Additionally, bacteria are able to multiply rapidly within
CSF because of the absence of effective host immune defenses. This is because normal CSF contains
few white blood cells (WBCs) and relatively small amounts of complement proteins and
immunoglobulins.
A critical event in the pathogenesis of bacterial meningitis is the inflammatory reaction induced by the
invading bacteria. Remember, that much of the pathophysiology of bacterial meningitis is a direct
consequence of elevated levels of CSF cytokines and chemokines.
The lysis of bacteria with the subsequent release of cell-wall components into the subarachnoid space
is the initial step in the induction of the inflammatory response and the formation of a purulent
exudate in the subarachnoid space
Chemokines (cytokines that induce chemotactic migration in leukocytes) and a variety of other
proinflammatory cytokines are also produced and secreted by leukocytes and tissue cells that are
stimulated by IL-1β and TNF-α.
Next slide please
TNF-α andIL-1β act synergistically to increase the permeability of the blood-brain barrier, resulting in
induction of vasogenic edema and the leakage of serum proteins into the subarachnoid space.
The subarachnoid exudate of proteinaceous material and leukocytes obstructs the flow of CSF
through the ventricular system and diminishes the resorptive capacity of the arachnoid granulations
in the dural sinuses, leading to interstitial edema. This can cause an increase of ICP that can explain
the symptom of headache experienced by the patient.
Neutrophil degranulation results in the release of toxic metabolites that contribute to cytotoxic
edema. This can explain the edema seen in the frontoparietal area and left occipital lobe of the
patient in his cranial CT scan. It also causes cell injury, and death that can explain the appearance of
her lacunar infarcts.
The combination of interstitial, vasogenic, and cytotoxic edema leads to raised ICP and coma.

For the Hematogenous seeding, bacteria colonize the nasopharynx and enter the bloodstream after
mucosal invasion. Upon making their way to the subarachnoid space, the bacteria cross the blood-
brain barrier, causing a direct inflammatory and immune-mediated reaction.

While in direct contiguous spread, Organisms can enter the cerebrospinal fluid (CSF) via neighboring
anatomic structures (otitis media, sinusitis), foreign objects (medical devices, penetrating trauma), or
during operative procedures.

These 2 pathophysiologic processes will start the inflammatory processes on the meninges causing
meningitis

Good morning, doctors! Today, December 4, 2021, we will be discussing trigeminal neuralgia.
Together with me are clinical clerks arnaiz, brazas, deocadez and lee with PGI abello and dillera and
residents in charge, dr. Amiscua, dr Dela cruz and dr Mercado.

DEFINITION
Trigeminal neuralgia is a syndrome characterized by paroxysmal facial pain. It is a chronic pain
condition characterized by recurrent brief episodes of electric shock-like pains, affecting the fifth
cranial (trigeminal) nerve, which supplies the forehead, cheek and lower jaw. This condition is almost
always unilateral and can involve one or more divisions of the trigeminal nerve.
The term “tic douloureux” was given by the French physician Nicolaus Andre in 1756, because of the
facial spasms, that can sometimes accompany the severe pain attacks.
Additionally, Dr. Godfrey Robeniol, a Neurology Consultant at the UP-Philippine General Hospital,
coined it as a suicide disease due to its unexplainable excruciating pain.
Dr. Robeniol explained that patients feel like being struck by lightning or a sudden stab on their face.
It could also be a hot painful feeling. Sometimes it last for just a second, sometimes it lingers for a few
minutes that even the air blow of electric fan triggers an attack. That’s why others commit suicide to
escape from this torturing agony

ETIOLOGY
Most cases of trigeminal neuralgia are due to the compression of the trigeminal nerve root, within a
few millimeters of its entry into the pons.
Between 80% and 90% of the cases are caused by compression by an adjacent artery or a vein.The
blood vessel, which has been mostly implicated in about 75% to 80% of the cases, is the superior
cerebellar artery. Other blood vessels that are known to cause TN include the anterior inferior
cerebellar artery, the vertebral artery, and the petrosal vein.

The trigeminal nerve, also known as the fifth cranial nerve, is the one responsible for the sensory
supply of the face and the motor and sensory supply to the muscles of mastication. The trigeminal
nerve starts at the pons and divides into three branches:

Ophthalmic (V1): Supplies the eye, upper eyelid, and the forehead
Maxillary (V2): Supplies lower eyelid, cheek, nostril, upper lip, and upper gum
Mandibular (V3): Supplies the lower lip, lower gum, jaw and the muscles of mastication

Some of the other causes of nerve compression include meningioma, acoustic neuroma, epidermoid
cyst, and rarely by an arteriovenous malformation or a saccular aneurysm.

Multiple sclerosis is a risk factor for TN, and it is reported in about 2% to 4% of patients with TN. This
is secondary to the demyelination of the trigeminal nerve nucleus by multiple sclerosis.[4]

EPIDEMIOLOGY
Trigeminal neuralgia affects 4 to 13 per 100, 000 people annually. AAFP journals stated that it affects
4.3 per 100, 000 of the population Women are affected more compared to men with a male-to-
female prevalence ratio of 1 is to 1.5 to 1.7. Most cases occur after age 50; some cases are seen in
second and third decades and very rarely seen in children. The peak incidence is at 60 to 70 years of
age, and classical trigeminal neuralgia is unusual before age 40 years. Trigeminal neuralgia is generally
sporadic, although there have been reports of the disease occurring in several members of the same
family. Spontaneous remission is possible, but most patients have episodic attacks over many years.
There is no racial predilection

The development of trigeminal neuralgia in a young person should raise suspicion for multiple
sclerosis. The prevalence in patients with multiple sclerosis is between 1 and 6.3%, making it the
most common associated disease. It is also reported that patients with hypertension have a slightly
higher incidence of TN compared to the general population.
These supports our consideration of trigeminal neuralgia for patient FS since she is a female, her age
of 70 years old, and her hypertension presenting w/ a unilateral R side pain upon chewing and lagging
of R eyelids.