Neurology Flashcards
pathway of CSF circulation
- Secretion
Choroid plexus in the ventricles (lateral ventricle mainly) - Circulation —
Lateral ventricle
V
Foramina of Monro
V
3rd ventricle
V
Aqueduct of Sylvius
V
4th ventricle
V
Foramen of Luschka and Magendie vessels
V
Subarachnoid space - Absorption
CSF is reabsorbed into venous circulation from subarachnoid spaces by arachnoid villi
the most common congenital cause of hydrocephalus
Aqueduct stenosis
Etiology of obstructive Hydrocephalus
Obstructive (non- communicating) hydrocephalus
1. Congenital
a. Aqueduct stenosis (the most common congenital cause): congenital stenosis or d
b. Dandy Walker malformation
Incomplete formation of the cerebellar vermis with obstruction of
foramina of Magendia and Luschka: Cystic expansion of th
ventricle with bulging occiput.
c. Vein of Galen malformation.
2. Acquired (the most common site of obstruction is at the aqueduct of Sylvius)
a. Traumatic: Posterior fossa subdural hematoma
b. Inflammatory post meningitic gliosis
c. Neoplastic: posterior fossa tumors e.g. cerebellar medulloblastoma
Etiology of communicating hydrocephalus
Congenital: Arnold- Chiari malformation
There is Failure of pontine flexure development > downward displacement of
medulla and cerebellum obstruction of subarachnoid space around the
brain stem usually.
Meningomyelocele is present in 80% of cases.
2. Acquired
a. Traumatic: subarachnoid hemorrhage.
b. Inflammatory post meningitic subdural adhesions
c. Neoplastic: choroid plexus papilloma overproduction of CSF
Clinical picture of Hydrocephalus
General examination:
3 skulls:
large head
sutures widely separated
anterior fontanelle widely opened
3 Skin
stretched skin
scalp veins: prominent
loss of hair
3 eye
sunset appearance
squint
vision impaire
back: meningocele or meningomyelocele in Chiari malformation
Neurological examination:
Spasticity, Hypertonia, Hyperreflexia, Paralysis
Delayed motor and mental development
investigations of Hydrocephalus
- CT scan (the most important): dilatation of the ventricular system
Obstructive hydrocephalus: dilatation only proximal to the site of obstruction
Communicating hydrocephalus: all ventricles are dilated - antenatal ultrasound screening.
Treatment of Hydrocephalus
Treatment
1. Surgical
a. Removal of cysts or tumors that cause obstruction e.g. (choroid plexus papillectomy)
b. Non removable causes shunt operation: ventriculoperitoneal shunt is the most common
- Acetazolamide: in non-progressive cases
Definition of Meningitis
Inflammation of the pia and arachnoid matter which might intervene with CSF circulation
Inflammation of the pia and arachnoid matter which might intervene with CSF circulation
Meningitis
Etiology of Meningitis
- Bacterial
a. During the first 2 months of life
B B hemolytic streptococci
Gram negative enteric bacilli : E coli
Listeria monocytogenes
b. From 2 month to 12 years
Hemophilus influenza type B
Pneumococci
Meningococci - Viral
a. Enteroviruses (e.g. echo virus, Coxsackie) are the commonest.
b. Epstein-Barr virus, adenoviruses and mumps. - Tuberculous meningitis
- Other rare causes:
a. Mycoplasma
b. Fungal infections
Source of infection of Acute bacterial meningitis
- Hematogenous dissemination from a distant site (nasopharynx) > choroid plexus
of the lateral ventricles > meninges and CSF.
2. Bacterial invasion from a contiguous focus (sinusitis, otitis media, mastoiditis)
Pathophysiology of Acute bacterial Meningitis
- Early: leukocyte infiltration and activation leading to release of inflammatory mediators. So, edema and endothelial damage and small infarctions occur.
- Later: fibrosis can lead to obstructive hydrocephalus.
Manifestations of increased intra-cranial tension
In infants
1. Bulging fontanelle and separated sutures: late signs.
In older children
1. Projectile vomiting.
2. Severe headache.
3. Blurring of vision (papilledema): late sign.
4. Abducent or Oculomotor nerve paralysis.
5. Hypertension with bradycardia and irregular shallow breathing (late signs)
B23
clinical picture of Acute bacterial meningitis
F CCII F
Fever: vomiting, letharg
coma
convulsions
Increased cranial tension
Meningial irritation: DIC
Focal neurological damage
B23
Manifestations of meningeal irritation
- Neck pain and rigidity: passive flexion of the neck is difficult and painful.
- Kernig’s sign: if the hip and knee joint are flexed at 90, extension of the knee will be limited.
- Brudzinski sign: if the neck is flexed— the hips and knees will be flexed too.
- Arched back (opisthotonus) : late sign
B24
Manifestations of neurological deficits
spasticity
parpalysis
deafness
blindness
squint
mental retardation
convulsions
reduced consciousness or even coma.
INV of acute bacterial meningitis
CSF examination
1. Differentiating bacterial meningitis from tuberculous and viral meningitis from table
2. Culture and sensitivity tests are essential: if bacterial infection is suspected
3. Detection of antigens (PCR) and antibodies (ELIZA) of viral infection
4. Ziehl-Nielsen staining of the CSF if TB meningitis is suspected
other investigations
1. CBC: marked leukocytosis with bandemia
2. Blood culture
3. Kidney functions test and electrolytes
4. Coagulation screen if DIC is suspected
5. If TB is suspected: chest X ray, tuberculin rest.
6. CT with contrast to detect meningeal enhancement
7. MRI brain for better visualization of cerebral infarcts.
Contraindications of lumbar puncture
- Cardiopulmonary instability
- Coagulopathy or thrombocytopenia
- Coma with (GCS less than 9)
- Marked increased intracranial tension
- Infections at the site of lumbar puncture.
Complications of Acute bacterial meningitis are common in
Common in pneumococcal infection than meningococcal infection
Complications of Acute bacterial meningitis
A. Early complications
1.C.N.S
Subdural effusion: (confirmed by CT)
Convulsions focal or generalized.
Cerebral abscess: confirmed by CT scan.
2. others
a. Disseminated intravascular coagulopathy.
b. Shock due to acute adrenal insufficiency.
c. Inappropriate antidiuretic hormone release resulting in hyponatremia.
d. septicemia
1. Hydrocephalus due to inflammatory obstruction of CSF pathways.
2. Subdural empyema that increases the intracranial tension.
3. Epilepsy due to focal infarctions and adhesions
4. Focal Neuro deficit Signs………..
Prevention of Acute Bacterial meningitis
- Vaccination
a. Infants in the first year of life: HIB vaccine (against Hemophilus influenza) and pneumococcal conjugate vaccines
b. Children: at 2-3 years of age.-Meningococcal polysaccharide vaccine - Chemoprophylaxis
Rifampicin in meningococcal nasopharyngeal carriers and household contact
Treatment of Acute Bacterial meningitis
Treatment:
A. supportive: ABC
CCI
=Care of coma
=Anticonvulsants: diazepam and phenobarbitone.
= IV fluid if meningitis is complicated by shock (otherwise fluid is restricted to minimize cerebral edema
Assisted ventilation if respiratory failure occurs.
B. Specific treatment
a. Antibiotics: IV for at least 10- 14 days (in neonates 3 weeks).
Neonates and infants below 2 months:-
Third generation cephalosporins e.g. Cefotaxime 200 mg kg/day plus ampicillin 100mg/kg/day.
Infants and children above 2_months:-
Third generation cephalosporin e.g. Cefotaxime 200mg/kg/day or ceftriaxone plus vancomycin
Dexamethasone in H influenza infection to decrease incidence of gliosis and hearing loss
C. Follow up to detect late complications e.g. Epilepsy and mental retardation
B26
Diffuse viral infection of brain parenchyma
Encephalitis
the most common that causes Encephalitis
Herpes simplex type 1 and type 2
