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128 Cards in this Set

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What are the RFs for embolic stroke? (n.b same as for development of atheroma)
Hypertension, fam Hx, smoking, diabetes.
What are the RFs for in-situ thrombosis eg a cranial thrombus?
- RFs for atheroma +
- Hyperviscosity/ polycythemia
- Thrombophilia eg Factor V Leiden (can't stop thrombus formation)
- Vasculitis eg SLE
- OCP
- Alcohol
What are the 3 RFs for left atrial thrombus formation?
1. AF
2. Mitral stenosis
3. Low cardiac output states, even without AF.
What are the three evolving stages of neuronal cell infarction?
1: 12-24 hrs 'Red neurons'- Neurons become vacuolised, eosinophilic, with nuclear changes (pyknosis/ karryorrhexis), and neutrophil infiltration.
2: 24hr - 2 weeks. Macrophage influx + clean up of necrotic tissue + reactive gliosis
3. ~2 weeks - Removal of all necrotic tissue, loss of normal structure + gliosis.
What are the warning signs of a stroke?
Patient themselves not usually aware (anosagnosia), relies on bystander-
Facial weakness/ droop
Arm weakness
Speech difficulty/ slurring
TIME to act.
What are the 2 broad patterns of cerebral infarction, outline one of them .
Haemorrhagic (red) and non-haemorrhagic (white/ anemic).

Haemorrhageic: multiple, confluent petechial haemorrhages. The bleeding is a result of reperfusion of damaged vessels, eihter through collaterals, or after dissolution of the initial embolus.
A venous infarct (eg thrombotic occlusion of superior sagittal sinus) will usually be haemorrhagic.

White infarct - thrombosis! no collateral blood flow to flood the ischemic tissue. Result is initially no change, and then after ~2 days, becomes pale soft and swollen... and within 10 days, becomes gelatinous and friable. Eventually, the tissue liquifies (21days), leaving a fluid filled cavity lined by dark gray tissue.
Once the CT head scan has been formed and non-haemorrhagic stroke has been identified, what are the five principles of management of ischemic stroke?
1. Thrombolysis eg tPa within 3 hrs.
2. If this doesnt work, or is not suitable for this patient --> mechanical thrombectomy.
3. Aspirin
4. Medical support eg prevention of infection and DVT (compression stockings, SC heparin). Prevention of cerebral oedema sufficient to cause brain herniation (Monitor fluids, IV mannitol --> diuretic). And nil by mouth until swallow assessed.
5. Stroke centre and rehabilitation.
What bleeds are associated with trauma?
Epidural and sub-dural:
Middle meningeal tear 2nd to skull fracture... and bridging vein tear with shearing force of brain movement (bridging veins are fixed to dura) respectively.
n.b subdural common in the elderly: brain atrophy- BV stretching + increased space for movement.
Also common in infants: thin walled BVs.
What bleeds are associated with cerebrovascular disease?
SAS (eg berry aneurysm rupture) and parenchymal bleeds (hypertensive rupture of small penetrating arteries).
A patient presents with abrupt onset contralateral hemiparesis, worsening over the last 45 minutes. He has a bad headache, and is losing consciousness.
Patient is a 65 year old alcoholic with poorly managed hypertension. What is your diagnosis and why?
Intraparenchymal haemorrhage/ haemorrhagic stroke:
- Most common in 60+
- Hypertension and Alcohol 2 RFs
- Onset was abrupt, worsening over half an hour to 1.5hrs.
- Patient was losing consciousness and had a headache (other sx is vomiting).
A 24-year-old man presents with a sudden onset headache in the night and on getting up finds that he has developed a complete ptosis on the left eye. The eye is also fixed dilated, and deviated 'down and out'. What cranial nerve is affected?
Knowing the location of this cranial nerve, is there a problem in the anterior or the posterior circulation?
Combined with the headache, what is a likely diagnosis?
CN III.
Posterior.
Expanding posterior communicating aneurysm.
36 year old man presenting with evolving weakness and numbness in his toes and feet, and milder sx in his hands. His Cranial nerves are normal. He has lost power and sensation in his hands. He has bilateral foot drop and loss of sensation to the midshin. What is the likely pathology?
The loss of sensation and power in a symmetrical fashion of all four limbs points to a problem in the peripheral nerve.The evolving nature suggests the problem is one of slowed conduction rather than acutal loss of nerve fibres... thus could be inflammatory/ a demyelinating neuropathy. Given the 5 month time period, likely to be a chronic inflammatory demyelinating polyneuropathy (CIDP).
What is CIDP?
An acquired immune mediated inflammatory disorder of the pNS. Closely related to Guillain-Barre syndrome, consdiered the chronic counterpart of the acute disease.
Present with weakness, numbnress, tingling, difficulty walking. There is areflexia, there may also be atrophy and fasciculations.
If the patient had autonomic dysfunction, they would also report orthostatic dizziness, bowel and bladder dysfunction adn cadiac problems.
Tx includes : corticosteroids (prednisone- can also cause depression), plasmapheresis (plasma exchange), IV immunoglobulin, +/- immunosuppresants.
A 70 year old man presents with 10 days of ataxia, and a dull occipital headache. He has nystagmus on right and left lateral gaze (bilateral), with a dysarthria.
He has longstanding COPD (20 cigs/ day), and recently has had some haemoptysis and weight loss. Where is the pathology?
What is a likely diagnosis?
Treatment?
Red flag = haemoptysis and eight loss --> lung cancer?
Ataxia + bilateral nystagmus + dysarthria --> cerebellar dysfunction.
Occipital pain --> edema/ increased pressure in cerebellum.
Metastatic deposit from primary bronchogenic carcinoma?
The most common cause of Sub arachnoid haemorrhage is rupture of a saccular (berry) aneurysm. What are some of the other types of aneurysm that can rupture and cause SAH?
- Mycotic
- Atherosclerotic
- Traumatic
- Dissecting

Other causes include: extension of a traumatic haematoma, rupture of hypertensive intra-cerebral haemorrhage into the ventricular system, vascular malformations and tumors.
What are the four congenital conditions associated with berry aneurysms? Note: mostly to do with CT disorder.
1. Polycystic kidney disease (AD).
2. Ehrlers-Danos vascular type (IV)
3. Marfans
4. Neurofibromatosis 1
What is hydrocephalus?
The dilatation of the ventricular system due to excessive CSF accumulation. Mostly due to obstruction of flow.
What is the function of the cerebral aqueduct/ aqueduct of Sylvius and what would happen if it were obstructed?
The cerebral aqueduct is within the mesencephaon (midbrain), and connects the third ventricle in the diencephalon, to the fourth ventricle, which is sandwiched between the pons and the cerebellum. An obstruction at the level of the cerebral aqueduct would result in hydrocephalus: dilataiton of the lateral and third ventricles. The fourth ventricle would be spared.
What are the four cardinal signs of SAH?
1. Sudden onset/ thunderclap headache (worst of your life)
2. Rapid LOC
3. Vomiting
4. Neck stiffness
What are some signs you can look for in a person with SAH?
Signs of meningeal irritation:
- Fever
- Kernig's sign: flex hip, try to extend the knee, prevented by inflammation of the lumbar theca.
- Brudzinski's sign: passive neck flexion results in involuntary flexion of the hips.
+ Subhyaloid haemorrhage due to rise in ICP and retinal venous pressure.
+ Focal signs determined by the site eg CNIII palsy from posterior communicating aneurysm, or bilateral lower limb paralysis with anterior communicating aneurysm.
What are some of the complications of SAH, divided into acute (increased ICP), chronic and sub-acute.
Acute- hydrocephalus, brainstem herniation and coma & neurogenic pulmonary oedema.
Chronic: re-rupture of the aneurysm, or persistent neurological deficits.
Sub-acute: VASOSPASM of an uninjured vessel, occurs in 30% and is the leading cause of delayed morbidity and death (leads to additional ischemia and infarction). + SIADH/ hyponatremia/ cerebral salt wasting, or vasospasm.
What are the seven principles of managing SAH?
1. Most crucial, keep the patient breathing --> protect airway.
2. Keep BP in safe ranges.
3. Phenytoin- prevent re-bleeding, pt is at risk of seizure.
4. Nimodipine- keep vessels patent (Ca2+ channel block), keep brain perfused.
5. Treat hydrocephalus: ventricular drainage.
6. Treat hypnatremia (SIADH/ CSWS)
7. Prevent PE (compression stockings)
Damage to pain-sensitive structures in the anterior and middle cranial fossae will project pain via what nerve and distribution?
CN V: facial nerve, in distrubution of V1, V2 V3 across the face.
Infratentorial structures transmit pain to what nerves and what dermatomes?
Project to the upper cervical nerves, and therefore pain is felt on the back of the head and neck (C2/3 dermatomes).
If a patient presents with headache and unintentional weight loss, what are 3 things you might suspect?
Cancer
Giant Cell Arteritis
Depression.
What headaches are aggravated by bending, lifting, sneezing or coughing?
What other symptoms might this patient have?
Any pathology with a raised ICP eg a mass lesion. THe mass lesion is believed to cause traction on pain sensitive structures including meninges and dural venous sinuses. THe headache is dull, non throbbing, moderate intensity, worseded by physical activity adn change in posture.
Other symptoms might include nausea and vomiting.
The headache is known to wake the patient from sleep (Does it wake you at night?) in 10%, and is often worst in the morning.
Who presents with 'cough' or 'exertion headaches, eg what is their underlying pathology?
About 10% of patients with cough headache have intracranial abnormalities, usually in the posterior fossa. The Arnold-Chiari malformation in particular presents this way. Increased ICP alone can also do this.
What is the possible explanation for a person presenting with symptoms of a mass lesion eg headache, worse with bending over, worse in the morning etc, who also has a fever and is tachycardic?
Patient may have an inflammatory mass such as a granuloma, abscess or rarely localized haemorrhagic viral encephalitis. These expand similarly to neoplasms.
Occasionally, a demoyelinating plaque of MS (tumefactive plaque) may present in this way, and you must question about any previous episodes of neurologic dysfunction that improved spontaneously (remitting/ relapsing MS, most common).
Match up the age group to the neoplasm (children, adults, elderly)
1. Metastatic neoplasm:
2. Posterior ranial fossa and SC neoplasms:
1. adults. (breast and lung are the most common, and 1/4 of patients with these cancers will have brain mets)
2. Children
Who is at a greater risk of cranial neoplasms than the the general population?
Neurofibromatosis: Acoustic neuroomas, cranial nerve neurilemoma's, glial neoplasms and meningioma's.
Tuberous sclerosis-
Radiation of fungal scalp infection.
What is the most common brain tumor?
Glioma's: And malignant astrocytoma leads the list.
What are the main Sx of brain tumors and what produces these symptoms?
Headache and seizures are the most frequent presenting symptoms. Associated focal neuro signs are related to their location, but are the result of mass effect, local tissue destruction, cerebral oedema, and increased ICP.
Confusion and mental status difficulties will occur in patients with large tumors, those that cross the corpus callosum and those with large associated edema.
What are the most common intiial symptoms of a patient with brainstem glioma?
Gait abnormalities, visual disturbances, weakness and headache. The weakness is caused by pyramidal tract dysfunction (present in ~80%). The visual disturbances manifest as horizontal diplopia.
The headaches can be caused by several mechanisms, including expansion of the brainstem with traction on surrounding meninges and varying degrees of hydrocephalus. These headaches often occur in the suboccipital region, but their location can vary and may extend into the upper cervical area. In some patients, there may be a periorbital component of headache pain. Focal weakness can involve the face as well as 1 or more limbs and is usually asymmetric.
Other common Sx include dysarthria, focal numbness, hearing loss, vertigo, tinnitus and personality changes.
Emesis: caused by tumor-related compression of the vomiting centre in the floor of the 4th ventricle.
THe cerebellar dysfunction is a result of damage to cotioc-ponto-cerebllar pathways, or the cerebellar peduncles. Contributes particularly to high incidence of nystagmus.
THe most frequent cranial nerve signs is a CN VII palsy --> facial weakness, unilateral (LMN?).
What tumors are aggressive, and which are slow growing?
Slow growing = meningioma's and neurilemmoma's. Cause relatively little dysfunction until late in the disease, as the brain can compensate in pace with the expanding compressive process.
Rapidly enlarging - Metastatic deposits and glioblastoma's : progressive loss of function over a short period of time (weeks to months). Occasionally, will cause SUDDEN loss of function, suggestive of a stroke. Usually the result of haemorrhage/ infarction of the core of the neoplasm, which may become necrotic due to outstripping it's blood supply. Oedema may also appear around certain neoplasms (notably mets), causeing rapid appearance of symptoms.
Herniation is where increased cranial pressure/ expanding masses create vectors of force that direct the brain matter out of it's normal compartment. What are the normal compartments, and what are the specific herniations?
The intracranial space is a closed chamber, with one outlet (the foramen magnum) and stiff dural membranes (the falx cerebri and the tentorium cerebelli) that divide the space into compartments. Depending on where they are located (supratentorial or infratentorial), expanding masses create vectors of force that are directed toward the paths that connect these intracranial compartments. For asymmetrical mass lesions in the cerebrum, can displace the cingulate gyrus under the falx cerebri (dura) --> Subfalcine herniation.
Similarly, pressure build up around the tentorium cerebelli can displace brain tissue either upward or downward, = transtentorial herniation (medial aspect of tempproal lobe is compressed).
The cerebellar tonsils/ infra-tentorial compartments can also be displaced into the foramen magnum, the connection with the vertebral canal.
How does a brain tumor actually cause headache?
Why is the pain worst in the morning?
The mass lesion causes an increased intracranial pressure, related to tumor size, rapidity of growth, ventricular system obstruction, venous obstruction etc. The displacement of pain-senstitive intracranial structures such as superficial cerebral blood vessels, meninges and some cranial and upper spinal nerves is what causes the actual pain.
The pain is worst in hte morning due to the
What is an anencephalocele?
A diverticulum of malformed CNS tissue extending through a defect in the cranium.
What is the cause of Cerebral palsy?
Hypoxic insults during the prental or peri-natal periods.
What is Chiari I?
Low lying cerebellar tonsils that extend into the vertebral canal: can obstruct CSF (hydrocephalus) or cause medullary compression. The herniation manifests as headaches and cerebellar symptoms. = the most common form.
What is Chiari II and what is it associated with?
Chiari II is a congenitally small posterior fossa, with a misshapening of the midline of the cerebellum, with downward extension of the vermis (versus the tonsils) through F.magnum. Chiari II patients are invariably also afflicted by lumbar myelomeningocele, leading to partial or complete paralysis below the spinal defect.
What is another word for myelomeningocele?
Spina bifida: Occurs when there is incomplete closing of the embyronic neural tube. Overlying vertebra are not fully formed and remain unfused, and if the opening is large enough, allows a portion of the SC to protrude through the opening. There may or may not be a fluid-filled sac surrounding it.

Anencephaly: when the portion of the neural tube that will become the cerebrum does not close. Absence of brain + calvarium, forebrain development is disrupted.
Encephalocele: when other parts of the brain remain unfused.
What is polymalgia rheumatica?
PMR, an inflammatory syndrome of pain/ stiffness in the neck, shouldersr and hips. Caused by WBC attack of the lining of the joints. Can be very sudden, or can occur gradually. Most sufferers wake up in the morning with pain in their muscles, may also have temporal arteritis (50% of patients with temporal arteritis also have PMR).
PMR usually goes away within a year or 2 after treatment (oral corticosteroids).
Temporal arteritis: severe headaches, scalp tenderness/ face or jaw soreness, distorted vision, fatigue.
Other sx: fatigue, lack of appetite, anemia, malaise.
What are the 2 events in initiation of a seizure?
Once the seizure is initiated, what sustains propagation? (propagation phase).
1. High frequency bursts of APs: due to long-lasting depolarization of neuronal membrane (influx of Ca2+). Opens VG-Na+ channels --> Na+ influx --> depol and gen of repetitive APs.
2. Hypersynchronisation: usually the RAS works to de-synchronise the cortex... hypersynchronisation results in "spike discharge".
The seizure propagates when there is sufficient recruitment of neurons such that there is loss of surrounding inhibition: the seizure can then propagate to contiguous areas (local cortical connections) and to distant areas (long commissural pathways eg corpus callosum).
What mechanisms are normally in place to prevent seizure initiation?
- Intact hyperpolarization
- Region of surrounding inhibition, created by inhibitory neurons.
BUT: if bursts are sufficiency, the repetitive discharge leads to increased extracellular K+, bluntening hyperpolarization and depolarizing neighbouring neurons. The depolarisation --> NMDA activation, amplifying the activation of neurons.
What is the definition of a seizure?

How does this relate to epilepsy?
A paroxysmal event, due to abnormal excessive and hypersynchronous discharge from a group of neurons.
Having a seizure does not mean you have epilepsy: epilepsy is the tendency to have recurrent unprovoked seizures. This is caused by a shift in the balance of excitation and inhibition within the CNS.
The process of epiloptogenesis involves endogenous factors, epileptogenic factors and precipitating factors. Give some examples of each.
1. Genetics can dictate your seizure threshold level. Can be lower in some people.
2. Epileptogenic factors:
- Trauma & Surgery: risk begins 1 year after and for 15 years thence.
- Stroke.
- Infections/ inflammation (encephalitis, meningitis).
- Abnormalities of CNS development eg hamartoma's, AV malformation, neuronal migration abnormalities.
- AD/ MS
- Intracranial mass lesions.
3. Precipitating factors:
- Psychological or physical stress
- Sleep deprivation
- Hormonal changes associated with menstrual cycle.
- Exogenous factors eg toxic substances, drugs/ drug withdrawal.
- Photsensitivity
- Metabolic abnormalities.
What is the protocol for seizure/ status epilepticus management?
1. Protect from injury (esp head), loosen restrictive clothing, do NOT try to suppress movement.
2. Maintain airway: recovery position + head tilt/ chin lift/ jaw thrust.
3. Asses for artificial airway, insert guedel or inflatable airway if needed.
4. Give O2 via hudson mask.
5. Establish IV access and take bloods.

Then, interrupt the seizure!
- Take BSL --> hypoglycemic? Administer glucose.
- Give thiamine if alcohol/ B12 def suspected.
- Correct hypotension with fluid.
- If nothings working, give rectal/ IM or IV diazepam/ lorazepam.
- If still not working, give IV infusion of phenytoin.
- If STILL no response, give IV phenobarbitol: monitor for hypotension and respiratory depression.
- As last resort, use general anesthetics (propofol, thiopentone).
What is the difference between Idiopathic & Symptomatic Epileptic syndromes?
Idiopathic- No underlying cause identified, seizures are the only sign of the condition. Good prognosis, easy to control.
Symptomatic- known abnormality of brain tissue/ cause, localised abnormalities are seen on diagnostic tests. Prognosis not as good, seizures harder to control.
If a person is having a temporal lobe seizure, what are some symptoms he might experience?
Deja Vu
Amnesia
Auditory sensations such as a sound or tune.
Gustatory sensations such as a specific taste.
Olfactory, such as a smell that is not physically present. Strong/ distinct.
Psychic sensations- an out-of-body feeling.
Dysphoric or euphoric- fear, anger etc.
A seizure in what part of the brain is most associated with status epilepticus?
Frontal lobe.
Symptomatic partial seizure syndrome can begin at any age, most commonly in adulthood. IT can involve an abnormality in aly of the four lobes. What kind of things could have caused the abnormality?
Stroke, abscess, tumor, cyst, infection or post-infectious scarring.
A child gets recurrent generalised seizures (grand-mal) with impaired cognitive function, what epilepsy syndrome is this (eg idiopathic, symptomatic, partial, generalised), what causes this syndrome, and what specifically could this syndrome be?
- Symptomatic Generalised.
- Widespread brain damage eg perinatal hypoxia.
- Lennox-Gastaut syndrome: affects children, multiple generalised seizures, cognitive dsyfunction.
WHen does a febrile seizure occur? What are the consequences?
Febrile seizures affect children between 6months and 6 years, usually in the first few hours of a febrile illness. They are usually brief (<2min) tonic-clonic seizures. They do not cause brain damage. Unless, they are prolonged eg >15minutes, in which case they are an emergency.
Risk of developing epilepsy only if:
1. Seizure is prolonged.
2. More than 1 seizure within 24hr.
3. Focal features during/ after the seizure.
What are the complications for an adult having recurrent seizures?
1. Progressive impairment of long term memory; esp in temporal lobe seizures (centre for memory).
2. Anxiety, depression, psychosis.
What are the essentials of epilepsy management?
1. Treatment of underlying condition.
2. Avoidance of precipitating factors.
3. Prophylactic tx eg medications or lesionectomy/ temporal lobotomy.
4. Addressing the psychosocial issues: educating, family support, support groups (Epilepsy Australia).
What are the guidelines with withdrawing anti-epileptic treatment
Once seizures are controlled, drug should be continued uninterrupted for 2-3 years. If seizure free, may attempt to withdraw treatment over several weeks- months (abrupt cessation can trigger withdrawal seizures). 2/3 of patients will remain seizure free.
What are the options for non-medical treatment?
~20-30% of patients do not respond to treatment. For these patients, there are 4 surgical options:
1. Lesionectomy: resection of the known lesion/ focus of seizures.
2. Temporal lobotomy (unilateral): for a patient with uncontrolled seizures, and known hippocampal sclerosis (MTLE). This is less than 1% of patients, but the cure rate is >50% for this group.
3. Section of the corpus callosum (hemispherectomy): prevent spread from one side to the other.
4. Vagus nerve stimulation: mechanism unknown.
What is the protocol with epilepsy and pregnancy?
The frequency of seizures in pregnancy remains unchanged for half, increased for a third, and decreased for a fifth. Epileptic mothers have an increased risk of foetal abnormalitiess (5-6%, double the normal rate of 2-3%). This is attributed to the teratogenic effects of anti-epileptic drugs (valproate and carbamazepine, anti-folate effect; recommended taking folate 3 months prior to conception). However the risk of the drugs is deemed less significant than the potential harm of an uncontrolled seizure for mother and fetus.
Phenytoin, phenobarbitol and primidone also act as enzyme inductors, resulting in accelerated vitamin K
A patient experiences generalized tonic-clonic seizures. He was prescribed Valproate, which was not particularly effective. He has been trialling Dilantin now for 3 months, with increasing doses to achieve seizure suppression. Last night he had a headache, and took 2 aspirin at 7 and then another 2 at 10. He has woken up today, and does not know where he is or what day of the week it is. He sits down to try and write an email to his boss, but finds himself struggling to construct meaningful sentences. What has happened to this patient?
n.b Dilantin = Phenytoin
Phenytoin has saturable pharmacokinetics. WIth higher doses the half-life increases leading to disproportionate increases in plasm concentrations. It is also 90% plasma boubnd, and there is compettitive binding with valproate and also salicylates, increasing free phenytoin concentration. Phenytoin also has a narrow therapeutic window (40-100microM), and it sounds here like he is suffering acute overdose of phenytoin as a result of his increasing phenytoin dose and the displacement from albumin by the presence of salicylate (aspirin). This causes marked confusion, with intellectual deterioration.
Other adverse effects of phenytoin include quite un-aesthetic things like hirsuitism, gum hyperplasia and nystagmus. And also ataxia, vertigo and headache.
What makes carbamazepine (Tegratol, Teril) a good 1st line treatment for partial seizures?
Carbamazepine works similarly to phenytoin, but has a lower incidence and severity of adverse effects. Side effects include dowsiness, dizziness, blurred vision and maybe ataxia.
What anti-epileptic drug should not be given to someone with liver disease?
Valproate: hepatotoxic.
What is the use of phenobarbital in seizure management?
Phenobarbital is a benzodiazepine, discovered in 1902 as a useful sedative and incidentally used in epileptics and found to reduce incidence and severity of seizures. It is no less effect than phenytoin or carbamazepine, but is less well tolerated. Sedation is a SE (but tolerance develops) and there is the risk of OD --> coma, respiratory and CVS failure.
In status epilepticus, fast acting benzo's such as diazepam or lorazepam are used IV. If this fails, phenytoin is used, or phenobarbital if that doesn't interrupt the seizure. Failing that, anaesthesia is last line (halothane, propofol, thiopentone).
Phenobarbital is also the first line choice for the treatment of NEONATAL seizures.
n.b: phenobarbital is also has potent hepatic enzyme induction, and was historically used for neonatal jaundice (until phototherapy was developed), and is stil used today in patient's with Gilbert's Syndrome to aid in the conjugation of bilirubin.
Compare the effects of benzo's and barbs on the GABAa Cl- channel.
Benzo's- increase frequency of Cl- channel opening.
Barbs - increase duration of Cl- channel opening (getting your hair done at the BARBer takes a long time- duration).
What use do benzodiazepines have in the management of epilepsy?
Fast-acting benzo's such as lorazepam or diazepam have use in status epileptics (IV/IM), as first line intervention. Long-acting benzo's such as clonazepam (Rivotril) are appropriate for long-term therapy, for all but tonic-clonic seizures. They can cause drowsiness and lethargy, but tolerance develops to this.
What is Vigabatrin?
A newer anti-epileptic, a GABA analogue that inhibits GABA transaminase (GAT), increasing effects of this inhibitory NT.
Tiagabine has similar effects (GAT-1 inhibtion) and is useful as an 'add-on' therapy for refractory partial seizures.
What does topiramate do, and what clinical uses does it have? (main 2?)
Unknown, but believed to have primary anti-epileptic and anti-migraine effect by its blockage of voltage gated sodium channels, augmentation of GABA activity, and antagonism of AMPA receptors. Can also inhibit carbonic anydrase, which rarely is significant enough to cause metabolic acidosis (can not reabsorb bicarb/ lose H+ effectively in proximal tubule).

Most frequently prescribed for the treatment of Migraine.
In children, it is indicated for the treatment of Lennox-Gastaut syndrome, a disorder that causes seizures and developmental delay.
Psychiatrists have used it to treat bipolar disorder, or augment other psychotropics, or to counteract the weight gain associated with anti-depressants.
What four things must a doctor take into account when writing a medical certificate approving an epileptic's application to drive?
1. Recent medical history
2. Type of seizures
3. Frequency
4. Attitude eg compliance.
When is it okay for a doctor to notify the Driver Licensing Authority about a rogue patient with epilepsy?
If the patient is not following medical advice about not driving, the doctor is protected from livil liability if 'acting in good faith'- must weigh up confidentiality vs public interest.
Can a person with epilepsy drive a taxi or commercial vehicle?
No. If they've ever had a seizure (apart from childhood febrile), unlikely to be allowed to drive a commercial vehicle.
What are some things you would look for when interpreting a brain scan?
1. Symmetry
2. Focal lesions eg an MS plaque, an infarct, a collection of blood or a tumor mass.
3. Cerebral ventricles - are they distended by hydrocephalus?
4. Extradural abnormalites eg focal collections of blood in epidural or subdural haemoatoma's, or a tumor of the meninges.
In a brain ultrasound, indicated for abnormalities in infacnts eg ischemic encephalopathy, infection, or developmental malformation, what things show up as echogenic, and what structures are sonolucent.
Solid tissue = echogenic eg Choroid plexus, haemorrhage or tumor.
Sonolucent = ventricles, SF and cysts.
Cranial ultrasound is really only informative in infants, and is best used for supra-tentorial haemorrhage or fluid collections, abnormality of a <6 week old spine, and some ischemia.
What is the primary indication for CT?
Acute change in mental status.
Other indications include acute truama, haemorrhage, or infection.
When performing a CT scan, when is there value in injecting a water-soluble contrast media?
- Better reolution of structures, and blood pool effect in hypervascular neoplasms, aneurysms and vascular malformations.
- Can also demonstrate breach of the BBB eg meningitis, ischemia, abscess, tumor.
Name two benefits and two disadvantages of CT?
Benefits: quick, accessible, good bone resolution.
Disadvantages: Huge radiation dose, children must be sedated, and the risk of allergic reaction to the IV contrast, (+ if full body, the contrast is nephrotoxic, not to be used in kidney failure).
CT is less sensitive and specific than MRI, but is COST EFFECTIVE. Good for trauma, acute haemorrhage, tumor, atrophy, hydrocephalus.
MRI is best however for bone: soft tissue distinction.
How does MRI work?
Transient excitation of H+ protons by the radiofrequency. The subsequent return to equilibrium (relaxation) results in release of Rf energy (echo), that is detected by the coils that deliver the Rf pulses and is transformed into an MR image. = A map of the distribution of H protons; the signal intensity is imparted by both the density of H+ ions and the differences in relaxation of H protons on different molecules.
What is traumatic tap?
When the needle in an LP punctures a vein behind the theca: can be prevented by stopping when you hear the 'Pop' as the needle passes through the theca/ enter the SAS?
The main side effect is headache: 10% of patient have persistent leakage of CSF, for days-weeks.
What is the primary cause of fevers in paediatric patients?
Self-limiting viral infections.
When is a full septic screen and antibiotic therapy indicated in an infant?
Any infant <1 month with a temp >38, or infants 1-3months with a temp >38.5.
Neonates have difficulty localising infection, hence full screen.
What are the most common organisms in infant/ neonatal infection?
Particularly susceptible to Group B strep and gram-negative enterics.
Group B strep is found in the vagina/ rectum of a quarter of pregnant women, and is the most common cause of life-threatening infection in newborns. About 1 out of 200 babeis born to GBS carrier mothers develop symptoms.
What are the 6 indications for immediate evaluation of a child?
1. Under 2 months old.
2. Constant whimper.
3. Dyspnea
4. Dysuria
5. Signs of meningits eg stiff neck, purpura, delirium/ can't arouse.
6. Rectal temp >40
IN examination of a child, there are several components assesed, including crying, reaction to stimulation from parent, skin colour, hydation, and response to social overture. What are the criteria for 'severe/ 5' in these categories.
Crying- weak, moaning, high pitched.
Response- continual crying, barely responds to parent.
Skin is cyanotic, pale, mottled.
Dehydrated: sunken eyes, dry mucous membranes.
- No smile, face dull and expressionless.
What is the definition of meningitis?
Inflammation of the leptomeninges (pia-arachnoid) + CSF within the SAS.
Match the organisms responsible for the following types of meningitis:
1. Acute pyogenic.
2. Aseptic.
3. Chronic
4. Nosocomial
5. Non-infectious
1. Bacterial.
2. Viral
3. TB, spirochetes, cryptococcus.
4. Multiple organisms, and MDR.
5. CHemical, malignant cells, drugs, blood following SAH.
What is the most common route of entry into the CNS for eg bacteria?
Haematogenous seeding eg in bacteremia.
What are the four routes of entry into the CNS?
1. Haematogenous, mainly arterial.
2. Implantation/ Direct entry eg with trauma.
3. Local extension eg from scalp abscess.
4. PNS migration to CNS eg rabies, herpes zoster.
What are the three most common organisms responsible for pyogenic meningitis? (NHS)
1. Neisseria menigitides (meningococcal)
2. Haemophilus influenzae (if very young and NOT vaccinated)
3. Strep pneumoniae (pneumococcal)
Chronic meningitis can be a result of spirochetal infection: what organism is this mainly referring to, and what signs should be looked for on examination.
THe main spirochete is TREPONEMA pallidum (syphillis). On exam, look for the chancres of primary syphilis, or for rash/ lymphadenopathy of secondary syphilis.
What 5 organisms can cause viral encephalitis ? (mild, self limiting fever, headache, vomiting, stiff neck
Mumps, HSV II, HIV, Epstein-Barr, Enteroviruses.
What are some features of tubercular meningitis?
Insidious onset, cranial nerve palsies, exposure.
What is the primary FUNGAL cause of meningitis, and how is it distinguished from the other fungal culprit?
Cryptococcus: common in HIV patients or the immunosuppressed.
Use India Ink to distinguish from candida (or serology).
A patient returns from a holiday in new zealand, where she has been swimming in the warm water of thermal hot springs. She has fever, headache and has vomited twice. What should be suspected?
The triad of fever headache and vomiting, as well as conjuring up enteric/ viral infections, should also arouse suspicion of meningitis. Her history of swimming in warm un-chlorinated water (a lovely place for amoeba) should make amoebic meningitis a favoured differential.
A 65 year old man is brought in by a buddy to the ED with fever, headache, and is losing consciousness intermittently. Is also complaining of a sore neck. He mentions that he had a cough and a fever a few weeks ago, but this is different. He is known round the traps as a bit of a booze-hound/ durry-slayer.
What are your differentials?
Fever, headache, LOC, stiff neck
1. Headache, LOC and stiff neck could all be the result of a cerebrovascular incident.
- SAH could present in this way, however he would probably be in more pain, as the headaches of SAH are excruciating. Vomiting is the other presentation of SAH. It would also be important to enquire about the onset of the headache, and whether he was doing anything eg straining (Increase in ICP, a third of cases). Other signs to look for would be CN III palsy (down and out), lower limb paralysis, or subhyaloid haemorrhage.
- Intraparenchymal haemorrhagae (haemorrhagic stroke) also presents with decreasing consciousness, headache (+ vomiting). This man also has 2 known RFs; age and heavy alcohol abuse (others = hypertension (primary RF) and cocaine).
- THe other likely cause in this patient is meningitis: he has the classic triad of FEVER, HEADACHE AND NUCHAL RIGIDITY. Other presenting symptoms include impaired consciousness (>75%), nausea and vomiting (>35%) and seizures/ hemiparesis. The presence of fever makes an infective/ inflammatory cause the most likely. In additoin, the greatest RF for pneumococcal pneumonia is a preceding episode of pneumococcal pneumonia, which is what the patient may be describing.
- If the patient has been a long time smoker, the cough a few weeks ago may be the new-onset cough of lung cancer, and the cause of his headache/ impaired consciousness/ stiff neck could be brain metastase's causing local expansion in the brain, expanding onto local structures causing pain, and compression of the RAS causing LOC.
Neisseria Menigitides accounts for half of all cases of pyogenic meningitis. True or False.

Meningitis is often a result of infection by normal tract, usually the genitourinary tract.
True.

False: often result of infection of the URT eg N.mening, Haemoph.Inf, Strep. Pneumon.
Outline the process of invasion of normal flora organism, entry to the CSF, survival, and immune response.
Normal flora of URT --> invade into intravascular space: polysaccharid capsule prevents phagocytosis, allows survival in blood stream. Blood reaches CSF, pili attachment to cerebral cpaillary endothelial cells --> migrate across, enter CSF. Survive with minimal immune host defences in CSF, can multiply rapidly. Inflammatory reaction induced, with lysis of bacteria and release of components into SAS --> inflammatory response and pus formation in SAS. Cytokines cause increased permeability of BBB- vasogenic oedema and leakage of plasma proteins into SAS = vasogenic oedema. Obstructs outflow of CSF --> obstructive/ communicating hydrocephalus with concomitant interstitial oedema. Leukocyte migration into CSF and degranulation results in release of toxic metabolites --> cytotoxic oedema worsening pressure build up, + cell injury and death. Eventually, combination of interstitial, vasogenic and cytotoxic oedema leads to increased ICP and coma.
What is the most common long term complication of meningitis?
hearing loss.
True or False: Multiple sclerosis is an inherited disease, where there is primarily damage to the axons which secondarily damages the myelin sheath, impairing conduction.
False. MS is an ACQUIRED disease, with preferential damage to myelin. The natural history of the disease is actually dictated by the limited regenerative capacity of the CNS, and secondary damage to the axons (inflammatory etc).
What is the strongest RF for dementia?
Age.
Age related disruption of cerebral neuronal circuits. Alzheimer's/ PD are sometimes considered accelerated aging.
Sally is a 35 year old irish lady, who is presenting with some lower leg weakness, and numbness that started in the feet and is ascending. She reports having problems with double vision a few months, that resolved spontaneously.
Omar is a 55 year old Papua New Guinean man, presenting with the same symptom developing over the last 24hrs, but also noting he's having trouble walking, and that his legs keep buckling.
What are the most likely diagnoses for these patients, considering their patient profile, and what tests should be performed.
Sally: The typical early presentations of MS include blurred vision, numbness, weakness in one or two of the extremieies, instability walking, tremors and problems with bladder control/ heat intolerance.
This presentation of bilateral ascending numbness in the feet is a characteristic complaint of new MS patients. This is most likely what Sally is presenting with as MS typically presents in the thirties (not >55), is more common in women, and increases in frequency the further away you are from the equator (related to sunlight, climate, vitamin D).
A sensory exam should be performed, and the most common findings in the 'numb' areas will be dorsal column signs eg reduction of vibration and proprioception, rather than pain/ light touch changes of the spinothalamic tract.
The incident of dipolopia several months ago is also suggestive of MS: this is a common symptom, due to either internuclear opthalmoplegia, or 6th cranial nerve palsies. This pretty much satisfies a diagnosis of MS: 2 incidences of neuro pathology in 2 different anatomically distinct body parts, in the course of 6 months. Other findings on examination would be muscle weakness, the result of an UMN lesion therefore associated with mild spasticity and hyperreflexia. The most common presentation is paraparesis (eg bilateral leg weakness).

Now to Omar: does not fit the bill for MS.
The disorder of Guillain-Barre syndrome is characterised by symmetrical weakness, affecting the lower limbs first and progressing rapidly in an ascending pattern. This manifests in ''rubbery legs'' that tend to buckle, with or without numbness/tingling. Over the course of a few days, the arms and facial muscles become affects, as can the lower cranial nerves, leading to bulbar weakness (dysphagia, trouble swallowing, drooling, respiratory difficulties).
On examination, there will be loss of proprioception, but also crucially, there will be AREFLEXIA. There can be deep aching muscle pains in the weakened muscles, compared to the pain of overexercising. Fever should not be present; if it is, another cause hsould be suspected. Patient may also describe general weakness and decreased consciousness. GBS is the acute form of the inflammatory poly-neuropathy syndrome, which has the chronic counterpart in CIDP. CIDP would not be suspected in this case (CIDP must have sx for > 8 weeks). Other Sx of CIDP are related to the chronic nature of the disease eg there may be muscule atrophy, fasciculations and loss of reflexes/ sensation.
What can be done to confirm a diagnosis of MS?
- Lumbar puncture and CSF analysis for signs of chronic NS inflammation (oligoclonal bands of IgG on electrophoresis- 75% of patients).
- Neuroimaging can be done, such as MRI for demeylination/ plaques. Or Gadolinium can be administered IV, as a contrast to highlight active plaques/ demonstrate historical lesions.
What is the MOA of ethosuxamide (emeside) and what is it used to treat?
Ethosuxamide blocks the T-type Calcium channels. THis is useful in decreasing AP generation in the thalamic neurons in diseases such as epilepsy. It is the first line drug for Absence seizures, in part because it lacks the hepatotoxicity of the alternative anti-absence drug Valproate. The main side effects of ethosuximide are GI (nausea, anorexia) and some CNS changes (fatigue, lethargy, mood changes).
In meningitis, what are four mechanisms by which the integrity of the BBB is compromised?
1. Glycopeptides from the cell walls of killed strep pneumoniae (get endocytosed by the membrane)
2. Extracellular proteases, degrade the ECM.
3. Pseudomonas auruginosa,
What 3 virulence factors are common to all three of N.Mening, H.Influenz and Strep.pneumon.
1. Capsule
2. IgA Protease
3. Autolysins (lyse the host cell).

N.Mening and H.Influenzae also have pilli (attachment and invasion of nasopharynx).
By nature of being gram-ve, N.Mening and H.Influenz also have Endotoxin and OMP: outer membrane protein.
Describe the difference in presentation between acute fulminant meningitis and subacute infection.
1. Acute fulminant illness progresses rapidly within a few hours, resulting in sudden onset of shock, purpura +/- coma, the result usually of meningococcal septicemia.
2. Subacute meningitis worsens over several days, presenting with the classic triad of fever, headache and nuchal rigidity. Other Sx include nausea and vomiting, photophobia, and neuro signs eg impaired consicousness, seizures and hemiparesis.
A 2 year old child presents with temp >38, looks pale and has just vomited. What must be excluded? What other sypmtoms might point you towards this diagnosis?

Would testing for Kernig's and Brudzinki's signs be a reliable diagnostic tool in this patient? What other sign of meningeal irritation could you look for?
Fever, pallor and vomiting: could be gastro, or a systemic infection, but could also be meningitis. Would look or signs of altered consciousness, listlessness, irritiability, and a high pitched crying ("meningeal cry"). Seizures occur in 40%.

No. These tests are not so obvious in children. A different sign would be OPISTHOTONOS, an arched back posture due to hyperextension/ contraction of the extensor muscles of the spine. This is most common in infants.

Rash is also present in 50%. + Signs of Increased ICP (papilloedema, CN palsies 3,4,6,8.
What are the complications/ long-term effects of meningitis?
1. Hearing loss: inflammatory exudate preferentially collects in the basal cistern, where it damages the 8th cranial nerve. Less commonly, can be caused by spread of infection to the cochlear.
2. Kidney damage, from the septic shock.
3. Neural damage: Mental retardation, seizures, vision problems, paralysis, personality changes.
4. Limb deformity/ amputations secondary to septic embolic and peripheral ischemia.
5. Death.
What tests should someone with suspected meningococcal infection have performed?
Blood and nasopharyngeal swab, for culture.
+ Bloods for FBC, and coagulation studies if petechiae/ frank bleeding is evident (DIC).
+ electrolytes: for hyponatremia (CNS injury can result in cerebral salt wasting syndrome, or SIADH: inapparopriate ADH secretion and fluid retention).
Once raised ICP is ruled out (CT or MRI), and LP is taken, what tests should be done on the CSF?
Cytology, virology, gram stain, Ziehls-Zieson stain (TB), India Ink stain (Cryptococcus- fungal meningitis).
What changes are seen in the CSF with pyogenic meningitis (parameters are appearance, opening pressure, predominant cell, glucose, protein, organisms)
Appears turbid. Opening pressure >200mmH2O. Predominant cell is polymorphs eg neutrophils. Glucose is down due to bacterial consumption (CSF: serum ratio <0.4).
Protein is VERY HIGH, due to increased permeability of the BBB (protein molecules enter) + tissue degeneration, obstruction of the CSF circulation
Which organism carries the highest mortality?
Pneumococcal meningitis. Mortality is 1 in 5, going up to 50-90% if severe neurological impairment is evident at time of presentation, or there is extremely rapid onset.
This meningitis is usually preceded by a respiratory illness <7 days prior. Look out for it!
What is the practice with empirical anti-biotics in menigitis?
Meningitis has a very low threshold for treatment: it is a potentially serious diseases, and the risk of treatment is low, therefore empirical therapy with benzylpenicillin or ceftriaxone (if patient is allergic to penicllin). AB can be modified if Ix identify the definitive organism. Also has been shonwn the 10mg IV dexamethasone improves outcomes, decreasing meningeal inflammation + decreasing neuro sequelae such as hearing loss.

SO: Ceftriaxone IV. If immunosuppressed, add Benpen or Ampicillin IV. and if Pneumococcal Ag assay of CSF is +ve for For G+ve diplococci, add VANCOMYCIN. Covers for penicillin and cephalosporin resistant s.pneumoniae.
What are the 2 different pneumococcal vaccines?
1. Prevenar (7-valent)- protects against 90% of serotypes, effective in children <2. Free to those cildren at risk (indiginous or with pre-disposing medical condtitions).
2. Pneumovax (23 valent): given to older children and adults.
Is there an effective meningococcal vaccine?
There are effective vaccines for serotypes A, C, Y & W-125, however B is the most common serogroup in austalia and no vaccine exists for this: it is poorly imunogenic and has structures identical to human cells (may induce immunopathology).
When must the HiB vaccine be administered?
2, 4, 6, and 12 months.
What is the difference in presentation of pyogenic versus viral/ aseptic meningitis?
Both present with headache, fever, nuchal rigidiity and malaise, however viral meningitis is far less likely to present with alterations in consciousness, seizures or focal neurological signs.
What are the three most common viruses responsible for VM?
1. Enteroviruses
2. HSV II
3. Arboviruses.
What are the findings on CSF examination in viral meningitis?
1. lymphocytic infiltrate
2. normal/ slightly elevated protein
3. Normal glucose
4. Normal to slightly elevated opening pressure
5. NO ORGANISMS.
What is the mangament of aseptic meningitis?
Primarily symptomatic: analgesic, anti-pyretic, anti-emetic. Normally self limiting over several days. Can give anti-virals in HSV men. Excellent prognosis.
Ependymoma's- arise where in children and where in adults. Consequences?
In children, found in 4th ventricle. Here, they cause obstructive hydrocephalus rather than invasion of the pons or the medulla. 5-10% of brain tumors in children.
In adults, form in the SC (spinal ependymoma).
CSF dissemination is common.
On histology, which of the glioma's has sheets of regular cells, with spherical nuclei and finely granular chromatin with a surrounding clear halo of cytoplasm.

N.b this tumor is mostly found in the cerebral hemispheres, with a predilection for white matter. Often have a history of several years of neuro symptoms eg seizures.
Oligodendroglioma. Adult tumor (40s-50s), good prognosis with treatment (5-10years).
Half of patients with temporal arteritis also suffer from what:
Polymyalgia rheumatica.
Young girl, develops band-like pain from the forehead (bilaterally) around to the occiput. Sometimes radiates to the neck. Lasts about 30 minutes. What type of headache.
Tension headahe, acute.
Chronic = 15days/ month, for >6months.
55 year old man, sudden onset of unilateral headache around the front of the face. Seeing double. Cause?
Temporal arteritis: patient >50yo. Unilateral, with visual disturbances. May also have fever/ malaise/ weight loss.

N.b headache + weight loss in a man > 50 is temporal arteritis or cancer.
What are the RFs for meningitis?
- Male
- Low SES
- Crowding
- Splenectomy
- Sickle cell disease
- Prev resp infection
- Alcohlism/ cirrhosis (impaired synthesis of proteins)
- Diabetes.
A patient with alcoholic cirrhosis presents with a febrile coma. What should be suspected and what should be done.
Bacterial meningitis: even if LP cannot be performed, commence prophylactic IV ampicillin with a 3rd gen cephalosporin (cephalexin).
What is spasticity a sign of eg clasp knife.
UMN lesion- exaggeration of stretch reflex.
What system is affected if a paitent demonstrates rigidity eg lead piping, cog-wheeling (describe each).
Extra-pyramidal system: eg Parkinson's disease.
Lead pipe: constant throughout range of motiom/.
Cog-wheel: result of superimposition of rigidity, on tremor --> ratchetlike interruptions, typically seen at the wrists.
What is the pathology behind paratonia?
Paratonia: limb stiffens in response to any contact. Degree increases with force exerted by the examiner.
Cause: frontal lobe, or diffuse brain damage.
What are the causes of a) resting tremor, and b) action tremor.
a) PD
b) Beta-agonists, nervousness or cerebellar disorders.