Neurology Flashcards
Recap - Outline the main roles of the
a) Frontal lobe
b) Temporal Lobe
c) Parietal Lobe
d) occipital lobe
Frontal - decision making, movement, executive function, personality.
Temporal - hearing (primary auditory cortex), memory and language, smell, facial recognition
Parietal - Sensory info
Occipital lobe - Vision
Recap - What are the main responsibilities for the
a) Brainstem
b) Cerebellum
brainstem - controls Heart and breathing rate, Blood pressure and GI function, as well as consciousness
Cerebellum - Muscle coordination, and balance
Recap - what are the two arteries that supply the brain?
Internal carotid
Vertebral arteries
What does the internal carotid artery branch off to supply?
branches off to create the Anterior cerebral artery, as well as posterior communicating artery to join the circle of Willis
After this the ICA continues on as the Middle cerebral artery, which supplies the lateral portions of the cerebrum.
What does the middle cerebral artery supply?
· MIDDLE CEREBRAL ARTERY—(huge artery) supplies majority of lateral surface of the hemisphere and deep structures of anterior part of cerebral hemisphere.
After entering the cranium through the foramen magnum, what branches does the vertebral artery give off? What do the 2 vertebral arteries then go on to do?
Give off Spinal arteries, supply the entire length of spine
Gives off The Posterior Inferior cerebellar artery - supplies cerebellum
also gives off a menigeal branch
But after this two vertebral arteries converge to form the basilar artery
What arteries branch off the basilar artery?
Superior cerebellar artery (SCA)
Anterior inferior cerebellar artery (AICA) - Both to supply the cerebellum
The Pontine arteries
What does the posterior cerebral artery go on to supply? What is it a branch of?
Supplies occipital lobe, posteromedial temporal lobes, midbrain, thalamus,
It is the terminal branch of the basilar arteries,
What does the anterior cerebral artery supply?
· ANTERIOR CEREBRAL ARTERY (supplies and runs over Corpus Callosum and supplies Medial aspects of Hemispheres (anteromedial aspects of the cerebrum)
What does the anterior cerebral artery supply?
· ANTERIOR CEREBRAL ARTERY (supplies and runs over Corpus Callosum and supplies Medial aspects of Hemispheres (anteromedial aspects of the cerebrum)
What is a stroke?
An acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology
What are the Two types of:
a) Strokes the in brain
b) Ischaemic events in the brain
Two kinds of stroke are ischaemic (85%) and haemorrhagic (15%)
The two types of ischaemic events in the brain are a Cerebral infarction (an ischaemic stroke) or a Transient ischaemic attack (TIA)
a TIA is not considered to be an actual stroke
Describe the epidemiology of strokes
- Average age is 68-75
- 3rd leading cause of death in the UK
- More common in Asian and black Africans
- More common in males
What are the different causes of an ischaemic stroke?
- Cardiac: atherosclerotic disease, AF, paradoxical embolism due to septal abnormality
- Vascular: aortic dissection, vertebral dissection
- Haematological: Hypercoagulability such as antiphospholipid syndrome, sickle cell disease, polycythaemia
What are the different causes of haemorrhagic strokes
Intracerebral: bleeding within the brain parenchyma:
- Trauma
- Cerebral amyloid
- Hypertension
Subarachnoid: bleeding between the pia and arachnoid matter
- Trauma
- Berry aneurysm
- Arteriovenous malformation
Intraventricular: bleeding within the ventricles
What are the risk factors for developing a stroke?
- Hypertension
- Smoking
- AF
- Vasculitis
- Medication e.g. hormone replacement therapy
If the anterior cerebral artery is affected in a stroke where in the body will be affected?
Feet and legs
If the middle cerebral artery is affected in a stroke where in the body will be affected?
- Hands and arms
- Face
- Language centres in the dominant hemisphere
If the posterior cerebral artery is affected in a stroke where in the body will be affected?
The visual cortex will be affected meaning the patient won’t be able to see properly
Where will symptoms happen in regards to the stroke?
- Symptoms will usually happen on the side contralateral to the stroke unless a brainstem stroke then both sides will be affected
What are the symptoms of a anterior cerebral artery stroke?
Contralateral hemiparesis and sensory loss more commonly affecting the lower limbs
What are the symptoms of a middle cerebral artery stroke?
- Contralateral hemiparesis and sensory loss with upper limbs > lower limbs
- Homonymous hemianopia
- Aphasia: if the affecting dominant hemisphere 95% of right handed people this is the left side
- Hemineglect syndrome if affecting the non-dominant hemisphere patients won’t be aware of one side
What the symptoms of a posterior cerebral artery stroke?
- Contralateral homonymous hemianopiawithmacular sparing
- Contralateral loss of pain and temperature due to spinothalamic damage
What are the symptoms of a vertebrobasilar artery stroke?
- Cerebellar signs
- Reduced consciousness
- Quadriplegia or hemiplegia
What is Weber’s syndrome and what are the symptoms of it?
- It is a midbrain infarct that leads to oculomotor palsy and contralateral hemiplegia
What are the symptoms of lateral medullary syndrome (posterior inferior cerebellar artery occlusion)
- Ipsilateralfacial loss of pain and temperature
- IpsilateralHorner’s syndrome: miosis (constriction of the pupil), ptosis (drooping of the upper eyelid), and anhidrosis (absence of sweating of the face)
- Ipsilateralcerebellar signs
- Contralateralloss of pain and temperature
What is used to classify stokes and how does it do it?
The Bamford classification and it categorises strokes based on the area of circulation affected
What are the different classifications in the Bamford classification?
- Total anterior circulation stroke
- Partial anterior stroke
- Lacunar stroke
- Posterior circulation stroke
What is a TACS?
total anterior circulation stroke
Blood vessel= anterior or middle cerebral artery
Criteria: all of
- Hemiplegia
- Homonymous hemianopia
- Higher cortical dysfunction
What is a PACS?
partial anterior circulation stroke
Blood vessel= anterior or middle cerebral artery
Criteria is any two of:
- Hemiplegia
- Homonymous hemianopia
- Higher cortical dysfunction
What is a lacunar stroke?
Blood vessel= perforating arteries
Criteria: there is no higher cortical dysfunction or visual field abnormality and there is one of:
- Pure hemimotor or hemisensory loss
- Ataxic hemiparesis
- Pure sensomotor loss
What is a PCS?
posterior circulation stroke
Blood vessel= Posterior cerebral or vertebrobasilar artery
Criteria:
- Cerebellar syndrome
- Isolated homonymous hemianopia
- Loss of consciousness
What is used to identify strokes in the community?
F- Face
A- Arm
S- Speech
T- Time (this is a stupid one because it is not a symptom just there to make the word fast)
What is used to identify strokes in hospital?
Recognition of Stroke in the Emergency Room (ROSIER) scale.
What are the criteria for the ROSIER scale?
- Loss of consciousness
- Seizure activity
New, acute onset of:
- Asymmetric facial/arm/leg weakness
- Speech disturbance
- Visual filed defect
When would a stroke be possible using the ROSIER scale and what would happen as result?
A stroke is possible if they have any of the criteria and hypoglycaemia has been excluded
WOULD REQUIRE URGENT NON-CONTRAST CT
- Aspirin 300mg stat (after the CT)
What are the intial investigations for a suspected stroke?
First line: non-contrast CT of head
ECG- to asses for AF
Bloods to look for hyponatremia/hypoglycaemia
Carotid doppler
What is the gold standard test for a stroke?
Diffusion weighted MRI is more sensitive but harder to obtain
What are the differentials for strokes?
- Hypoglycaemia
- Hyponatremia
- Hypercalcaemia
- Uraemia
- Hepatic encephalopathy
What is the treatment for a ischaemic stroke?
- Antiplatelets: aspirin given as soon as possible once haemorrhagic stroke is excluded
- Thrombolysis: alteplase (tissue plasminogen activator)- given if to re-establish blood flow is <4.5 hours of symptom onset
- Thrombectomy must score > 5 on NIH Stroke Scale/Score (NIHSS) and pre-stroke functional status < 3 on the modified Rankin scale
What should be performed before thrombectomy?
CT angiogram (CTA):identifies arterial occlusion
What is given for the prevention of ischaemic strokes?
- Clopidogrel an antiplatelet
- High dose staitn
- Carotid stenting
- Manage underlying risks
What is the treatment for a haemorrhagic stroke?
- Related to the subtype of haemorrhage which will cover later
But for now:
- Admit to neurocritical care:patients will need intensive monitoring
- If features of raised intracranial pressure: consider intubation with hyperventilation, head elevation (30°) and IV mannitol
- Surgical intervention:decompression may be needed
What is the prognosis for a stroke?
For ischaemic stroke, the prognosis depends on the severity. A total anterior circulation stroke confers the poorest prognosis. Regarding thrombolysis, if administered within 3 hours, patients are 30% more likely to have minimal or no disability.
In general, mortality for haemorrhagic stroke is significantly higher than for ischaemic stroke and can be as high as 40%.
What are the driving rules after a stroke?
- Must not drive for 1 month after a stroke and can’t drive a HGV for 1 year after a stroke
What is a TIA?
- A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction.
- It usually resolves within 24 hours
What are the symptoms of a TIA in the internal carotid artery?
ACA: weak numb contralateral leg
MCA: body, face drooping w/forehead spared, dysphasia (temporal)
PCA -Homonymous hemianopia: visual field loss on the same side of both eyes
Hemisensory loss
Amaurosis fugax
What are the symptoms of a TIA in the vertebral/ basilar arteries
Diplopia – double vision
Vertigo
Vomiting
Choking and dysarthria
Ataxia
Hemisensory loss
what score can help stratify which patients are at a higher risk of a stroke following a TIA?
ABCD2 score:
A: age greater than 60
B: Blood pressure greater than 140/90
C: clinical feature: Unilateral weakness (2 points), speech disturbance (1 point)
D- Diabetes
D- Duration 60 minuets or longer (2 points) 10 to 59 (1 point)
High risk:
ABCD2 score of 4 or more, AF is present, More than TIA in one week or a TIA whilst on anti-coagulation
Low risk:
None of the above
Present more than a week after their last symptoms have resolved
What are the primary investigations for a TIA?
- Auscultation: listen for carotid bruit
- CT scan - Request an urgent CT scan of the head
- Carotid doppler – look for stenosis
- CT angiography – look for stenosis
What is the management for a TIA?
- First line is antiplatelet initially with aspirin 300mg
- Carotid endarterectomy: surgery to remove blockage of >70% on doppler
- Manage cardiovascular risk with atorvastatin etc
What is a crescendo TIA?
Where there are two or more TIAs within a week. It carries a high risk of a stroke
How many people who have a TIA will go on to have a stroke?
10% within 3 months
What are the two categories a haemorrhagic stroke can be split in to?
- Intracerebral where the bleeding occurs within the cerebrum
- Subarachnoid when bleeding occurs between the pia and arachnoid matter
What can cause an intracerebral haemorrhage?
- Hypertension causing arteriosclerosis and microaneurysms called bouchard aneurysms
- Arteriovenous malformations blood vessels that directly connect an artery to a vein
- Vasculitis/Vascular tumours
- Secondary to an ischaemic stroke- ischaemia causes brain tissue death. If there is reperfusion there’s an increased chance that the damaged vessel might rupture
What are the risk factors for developing an intracerebral haemorrhage stroke?
- Head injury
- Hypertension
- Aneurysm
- Brain tumour
- Anticoagulant
Describe the pathophysiology of an intracerebral haemorrhage?
- Once blood starts to spew from damaged vessel it creates a pool of blood that increases pressure in the skill and puts pressure on nearby cells and vessels. This can also lead to brain herniation
- Haemorrhage also results in less blood flowing downstream to cells. The pressure or lack of blood can lead to tissue death within hours
What are the presentations of an intracerebral haemorrhage?
- Sudden headache is a key feature
- Weakness
- Seizure
- Vomiting
- Reduced consciousness
What are the investigations for a intracerebral haemorrhage?
- CT/MRI to confirm size and location of the haemorrhage
- Check FBC and clotting
- Angiography to visualise the exact location of the haemorrhage
What is the management for a intracerebral haemorrhage?
- Consider ICU and intubation and ventilation if there is reduced consciousness
- Correct any clotting abnormalities
- Correct severe hypertension but avoid hypotension
- Drugs to relieve intercranial pressure mannitol
What are the surgeries that can be performed for an intracerebral haemorrhage?
- Craniotomy part of the skull bone is removed to drain any blood and relieve pressure
- Stereotactic aspiration: aspirate off blood and relieve intracranial pressure guided by a CT scanner. Good for bleeding that is located deeper in the brain
Describe the epidemiology of a subarachnoid haemorrhage?
- Most common in people 45-70
- More common in women
- More common in black patients
What can cause SAH?
- Trauma is a key factor
- Atraumatic cases are referred to as spontaneous SAH
What is the most common cause of a spontaneous SAH?
- Berry aneurysm- they account for 80% of cases.
- Arise at points of bifurcation within the circle of Willis; the junction between the anterior communicating and anterior cerebral artery
- They are associated with PKD, coarctation of the aorta, and connective tissue disorders (Marfan)
What are the risk factors for having a SAH?
- Cocaine use
- Sickle cell anaemia
- Connective tissue disorders
- Neurofibromatosis: tumours form on your nerve tissues
- PKD
- Alcohol excess
What can occur as a result of a subarachnoid haemorrhage?
- Blood vessels that are bathing in a pool of blood can start to intermittently vasoconstrict (vasospasm) called. If this occurs in the circle of Willis it will reduce the supply of blood flow to the brain causing further injury .
- Over time blood in the subarachnoid space can irritate the meninges and cause inflammation which leads to scarring of the surrounding tissue. The scar tissue can obstruct the normal outflow of CSF causing fluid to build up leading to hydrocephalous
What are the signs of a SAH?
- 3rd nerve palsy- if the aneurysm occurs in posterior communicating artery
- 6th nerve palsy a non-specific sign which indicates raised intercranial pressure
- Reduced GCS
What are the symptoms of a SAH?
- Thunderclap headache during strenuous activity or sex. It’s like being hit really hard on the back of the head
- Neck stiffness
- photophobia
- Vison changes
What are the initial investigations for SAH?
- FBC
- Serum glucose
- Clotting screening
- Urgent non-contrast CT of the head. Blood will cause hyperattenuation (this means becoming more dense on CT will show as white) in the subarachnoid space
What tests would you perform if CT is negative but a SAH is still suspeccted?
- Lumbar puncture: will show RBCs or xanthochromia (yellow pigmentation due to degradation of haemoglobin to bilirubin)
What is the management to prevent vasospasm?
Nimodipine is a CCB and prevents vasospasms
What is the management to stop the bleeding?
SAH
- first-line is endovascular coilingof the aneurysm;
- second-line is surgical clippingvia craniotomy
- If features of raised intracranial pressure: consider intubation with hyperventilation, head elevation (30°) and IV mannitol
What are the complications of a SAH?
- Rebleeding 22% risk at one month
- Vasospasm: accounts for 23% of deaths; at highest risk for the first 2-3 weeks after SAH; treated with (induced) hypertension,hypervolemia andhaemodilution (triple-H therapy).
- Hydrocephalus: acutely managed with external ventricular drain (CSF drainage into an external bag) or a long-term ventriculoperitoneal shunt, if required
- Seizures: seizure-prophylaxis is often administered (e.g. Keppra)
- Hyponatraemia: commonly due to syndrome of inappropriate antidiuretic hormone secretion (SIADH)
What is the prognosis for SAH?
At 6 months, 25% of patients are dead and 50% are moderately to severely disabled.
Causes of mortalityinclude medical complications (23%), vasospasm (23%), rebleeding (22%) and initial haemorrhage (19%)
What is a subdural haemorrhage?
Bleeding below the dura matter
Who is most likely to suffer from a SDH?
- Elderly
- Alcoholics
What can cause a SDH?
- Brain atrophy: in the elderly the brain shrinks in size meaning the bridging veins are stretched across a wider space where they are largely unsupported
- Alcohol abuse: causes the wall of veins to thin out making them more likely to break
- Trauma/injury: falls, shaken baby syndrome, acceleration-deceleration injury
What is a haematoma and how do they cause issues?
The collection of blood that forms as a result of a haemorrhage.
As damaged bridging veins are under low pressure, the bleeding can be slow causing a delayed onset of symptoms as the haematoma gradually increases in size. Over time this will compress that brain and increase intercranial pressure
What is an acute SD haematoma?
One that causes symptoms within 2 days
What is a subacute SD haematoma?
One that causes symptoms between 3-14 dyas
What is a chronic SD haematoma?
One that causes symptoms after 15 days
What are the symptoms of a SDH?
- Reduced GCS: which can occur straight away or in the ensuing days and weeks as the haematoma increases in size
- Headaches
- Vomiting
- Seizures
What are the investigations for a SDH?
Immediate CT head
What will an acute SDH look like on a CT?
A hyperdense mass more white than the surrounding healthy brain tissue
What will an acute SDH look like on a CT?
A hyperdense mass more white than the surrounding healthy brain tissue
What will a chronic SDH look like on a CT?
A hypodense mass less white than the surrounding healthy brain tissue
What shape does a subdural haematoma show as on a CT?
Bleeding is between the dura and the arachnoid so it follow the contour of the brain and dorms a crescent shape and cross suture lines.
What are the differentials for a SDH?
- Stroke
- Dementia
- CNS masses e.g. tumours or abscesses
- Subarachnoid haemorrhage
- Epidural haemorrhage
What is the management for a SDH?
Drainage:
- small SDH are drained via a burr hole washout a small tube called
- large SDH requires a craniotomy which is when part of the skull bone is removed
- IV Mannitol to reduce ICP
What are the complications a the raised intercranial pressure in a SDH?
- Supratentorial herniation: cerebrum is pushed against the skull or the tentorium, can compress the arteries that nourish the brain leading to an ischaemic stroke
- Infratentorial herniation: cerebellum is pushed against the brainstem, can compress the vital area in the brainstem that control consciousness, respiration, and heart rate
What is an epidural haemorrhage?
Bleeding above the dura matter
Who is an EDH most common in?
They usually occur in young adults
What is the most common cause of a EDH?
It is most commonly caused by head trauma. The meningeal arteries are protected by the skull but can be damaged by serious head trauma
Where is the most common site for a EDH to occur?
The Pterion which is the spot where the frontal, parietal and temporal and sphenoid bone join together.
It is a thin area of the skull and located just above the middle meningeal artery
What happens once the meningeal artery ahs been torn?
Blood will pool between the skull and the external layer of the dura mater, separating it from the inner surface of the skull. The blood builds up between the skull and the outer layer of the dura mater but cannot cross the suture lines where the dura mater adheres more tightly.
If blood accumulates slowly, there may be a lucid interval which is when several hours pass before the onset of symptoms.
What are the symptoms of a EDH?
-
Reduced GCS: loss of consciousness after the trauma due to concussion
- There might be a lucid interval after initial trauma if there is a slower bleed. This is followed by rapid decline.
- Headaches
- Vomiting
- Confusion
- Seizures
- Pupil dilation if bleeding continues
What will a EDH look like on an CT scan?
Hyperdense mass = looks “more white” than the surrounding healthy brain tissue.
What shape will an EDH be on a CT scan?
Epidural haemorrhages cause blood to build up between the outer layer of the dura mater and the skull.
Epidural haematomas don’t cross suture lines and they push on the brain forming a biconvex shape.
What are the differentials for a EDH?
- Epilepsy
- Carotid dissection
- Carbon monoxide poisoning
- Subdural haematoma
- Subarachnoid haemorrhage
What is the management for a EDH?
-
Clot evacuation
- Craniotomy: part of the skull bone is removed in order to remove accumulated blood below.
- Followed by ligation of the vessel.
- IV mannitol to reduce ICP
What is Cushing’s reflex?
physiological nervous system response to increased intracranial pressure (ICP) that results in Cushing’s triad of:
- increased blood pressure
- irregular breathing,
- bradycardia.
What is the meningitis?
Inflammation of the leptomeninges (the arachnoid and pia) and usually occurs due to a bacterial or viral cause
What are the most common cause of bacterial meningitis?
- S.pneumoniae
- N. meningitidis
What is the most common cause of viral meningitis?
- Enteroviruses such as coxsackievirus
- Herpes simplex virus (HSV)
- Varicella zoster virus (VZV)
What are the causes of fungal meningitis?
- Cryptococcus neoformans
- Candida
What is the most common cause of bacterial meningitis in neonates?
Group B streptococcus (GBS) S. agalactiae usually contracted during birth from the GBS bacteria that can often live harmlessly in the mothers vaginas.
What are some risk factors for developing meningitis?
- Immunocompromised: such as being in the extremes of age, infection (HIV), and medication (Chemotherapy) Listeria monocytogenes
M. Tuberculosis - Non-immunised: at risk ofH. influenza, pneumococcal and meningococcal meningitis
- Crowded environments: students living in halls of residence are a commonly affected demographic
What are the two routes of infection for meningitis?
- Direct spread
- Hematogenous spread
How can meningitis spread directly?
- Pathogens get inside the skull or spinal column and penetrate the meninges
- Sometimes the pathogen will have come through the overlying skin or up through the nose but more likely through anatomical defect or acquired like a skull fracture
How does meningitis spread via the blood?
- Pathogens enter the blood stream and move through the endothelial cells in the blood vessels making up the blood brain barrier
What happens once the pathogen causing meningitis reaches the CSF?
- Once in CSF pathogen will start multiplying, This will cause WBC in CSF to release cytokines and recruit additional immune cells. This will massively increase the number of WBC in CSF
- Additional immune cells will attract more fluid to the area and start causing local destruction this will cause CSF pressure to rise
- Immune reaction will cause the glucose concentration of the CSF to fall and protein level increase
What types of meningitis are acute and which are more commonly chronic?
- Bacterial and viral meningitis are usually acute
- Fungal is more chronic
What are the two tests to look for meningeal infection?
Kernigs Test
Brudzinski’s Test
What is Kernigs Test?
- Involves patient lying on their back and flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed. This causes the meninges to stretch
- A positive test will be where there is spinal pain or resistance to the movement
What is Brudzinski’s Test?
- Involves lying a patient on their back and gently using your hands to lift their head and neck off the bed and flexing their chin to their chest
- A positive test is when a patient involuntarily flexes their hips and knees
What is another classic sign of meningococcus meningitis?
. non-blanching rash” that everybody worries about as it indicates the infection has caused disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages.
Other causes of bacterial meningitis do not cause this rash
What are the symptoms of meningitis?
- Headache
- Photophobia
- Neck stiffness
- Fever
- Nausea vomiting
- Seizures
What are the primary investigations for meningitis?
- FBC:leukocytosis
- CRP:raised inflammatory markers
- Coagulation screen: required prior to lumbar puncture (LP)
- Blood glucose: required in all patients and for comparison with CSFglucose
- Blood culture:positive in the case of bacterial infection
- Whole-blood PCR forN meningitidis
What is the main investigation for meningitis?
Lumbar puncture
What are some contraindications for a lumbar puncture?
Raised ICP
GCS <9
Focal Neurological signs
Where is a lumbar puncture usually taken from?
Between L3/L4
Since spinal cord ends L1/2
What will a lumbar puncture show for different types of meningitis?
- Bacteria will release proteins and use up glucose
- Virus don’t use glucose but may release small amounts of proteins
The immune system releases neutrophils for bacterial and lymphocytes for viral
What is used to treat patients in primary care with suspected meningitis and a non-blanching rash?
(IM or IV) of benzylpenicillin prior to transfer to hospital as time is so important:
< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg
This shouldn’t delay transfer. Where there is a true penicillin allergy transfer should be the priority rather than other antibiotics.
How would you treat bacterial meningitis in hospital?
Ideally a blood culture and a lumbar puncture for cerebrospinal fluid (CSF) if the patient is acutely unwell antibiotics should not be delayed.
There should be a low threshold for treating suspected bacterial meningitis, particularly in babies and younger children. Always follow the local guidelines however typical antibiotics are:
< 3 months – cefotaxime plus amoxicillin (the amoxicillin is to cover listeria contracted during pregnancy from the mother)
> 3 months – ceftriaxone
Vancomycin should be added to these if there is a risk of penicillin resistant pneumococcal infection such as from recent foreign travel or prolonged antibiotic exposure.
Dexamethasone is given 4 times daily for 4 days to children over 3 months if the lumbar puncture is suggestive of bacterial meningitis. to reduce chances of neurological symptoms afterwards
What is the treatment for viral meningitis?
- Conservative management is appropriate most of the time
- Give Aciclovir if HSV or VZV
Is meningitis a notifiable disease?
Yes obviously the only reason this question is in here is so I can say that it is
What are the complications of meningitis?
- Hearing loss
- seizures and epilepsy
- Cognitive impairment
- Memory loss
- Limb weakness or spasticity
What is encephalitis?
Inflammation of the brain parenchyma. It mostly affects the frontal and temporal lobes
What is the main cause of encephalitis?
The herpes simplex virus HSV-1 accounts for 95% of cases from cold sores.
In neonates HSV-2 from genital herpes is the most common
What are some risk factors for developing encephalitis?
- Immunocompromised
- Blood/fluid exposure: HIV and west Nile virus
- Mosquito bite: west Nile virus
- Transfusion and transplantation: CMV, EBV, HIV
- Close contact with cats: toxoplasmosis
What causes encephalitis?
- An immune response to an invading pathogen
- HSV gets into the sensory ganglia by travelling retrograde from skin and recurrent infection happens when it travels anterograde back to the skin. I
- If it travels to the CNS, it leads to encephalitis. This is usually along olfactory or trigeminal nerves.
Where are the signs of encephalitis?
- Pyrexia
- Reduced GCS
- Aphasia
- Hemiparesis
- Cerebellar signs
What are the symptoms of encephalitis?
- Fever
- Headache
- Fatigue
- confusion
What are some behavioural changes that occur in encephalitis?
- Memory disturbance
- Psychotic behaviour
- Withdrawal or change in personality
What are some investigations for encephalitis?
- Throat swab
- HIV serology
- MRI of head will show evidence of inflammation will be normal in 1/3 of cases
- Lumbar puncture and CSF investigation including a PCR for HSV
What are some differentials for encephalitis?
- Meningitis
- Encephalopathy
- Status epilepticus
- CNS vasculitis
What is the treatment for encephalitis?
- Aciclovir should be given in all cases where it is suspected
- Ganciclovirmay be preferred in other herpesvirus infections, such as HHV-6
What is the prognosis for encephalitis?
Untreated HSV encephalitis is associated with a 70% mortality. This is significantly reduced with early antiviral therapy.
Survivors often have neurological sequelae such as short-term memory impairment and behavioural changes
What is MS?
An autoimmune cell-mediated demyelinating disease of the central nervous system
What is the epidemiology of MS?
- More common in women
- 20-40 most common age for diagnosis
- More common in white
- More common in northern latitudes
Symptoms will improve in pregnancy and post-partum period
What are some risk factors for developing MS?
- Vitamin D deficiency
- Family history: HLA-DR2 is implicated; 30% monozygotic twin concordance
- EBV infection: the virus with the greatest link to MS
- Smoking
- Obesity
Describe the pathophysiology of MS
- T-cells get through the blood brain barrier and are activated by myelin. The T-cell then changes the BBB to allow more immune cells to get in the brain
- MS is a type IV hypersensitivity reaction: T-cells release cytokines and these recruit more immune cells whilst also damaging the oligodendrocytes.
- B-cells will make antibodies that will destroy the myelin of the e oligodendrocytes. leaving behind areas of plaque/sclera
How does MS progress over time?
In early disease, re-myelination can occur and symptoms can resolve. In the later stages of the disease, re-myelination is incomplete and symptoms gradually become more permanent.
A characteristic feature of MS is that lesions vary in their location over time, meaning that different nerves are affected and symptoms change over time
MS lesions change location over time is that they are “disseminated in time and space”.
What are the different types of MS?
- Relapsing-remitting:
- Secondary progressive
- Primary progressive
- Progressive relapsing
- Clinically isolated syndrome (kind of counts)
What is Relapsing-remitting: MS?
- The most common pattern 85% of cases
- Episodic flare-ups separated by periods of remission. There isn’t full recovery after flare ups so disability increases over time.
60% will develop secondary within 15 years
What is secondary progressive MS?
Initially, the disease starts with arelapsing-remitting course, but then symptoms get progressively worse withnoperiods of remission
What is primary progressive MS?
- Symptoms get progressively worse from diseaseonsetwithno periods of remission
- Accounts for 10% of cases and is more common inolder patients
What is Progressive relapsing MS?
- One constant attack but there are bouts superimposed during which the disability increases even faster
What is clinically isolated syndrome MS?
- This describes the first episode of demyelination and neurological signs and symptoms. MS cannot be diagnosed on one episode as the lesions have not been “disseminated in time and space”.
- Patients with clinically isolated syndrome may never have another episode or develop MS. If lesions are seen on MRI scan then they are more likely to progress to M
What are the signs and symptoms of MS?
- Optic neuritis
- Eye movement abnormalities- double vision VI nerve
- Focal weakness (incontinence, limb paralysis, Bells palsy)
- Focal sensory symptoms ( numbness, pins and needles, Lhermitte’s sign is an electric shock sensation that travels down the spine and into the limbs when flexing the neck.)
- Ataxia
- Uhthoff’s phenomenon: worsening of symptoms following a rise in temperature, such as a hot bath
What is optic neuritis?
Demyelination of the optic nerve which present with:
- Unilateral reduced vision
- Central scotoma (enlarged blind spot)
- Pain on eye movement
- Impaired colour vision (red)
What is the primary investigation for MS and what would it show?
MRI of brain and spine:
- Will show demyelinating plaques called Dawson’s fingers
- High signal L2 lesions
- Old lesions willnotenhance with contrast, whereas newer lesions will. This provides evidence of dissemination of lesions in time and space which is required for a diagnosis of MS
What is the diagnostic criteria used to diagnose MS?
McDonald criteria
What is the McDonald criteria based on?
2 or more relapses and either:
- Objective evidence of two or more lesions
- Objective evidence of one and a reasonable history of a previous relapse
‘Objective evidence’ is defined as an abnormality on neurological exam, MRI or visual evoked potentials
What is used to treat a MS relapse?
- Oral or IV methylprednisolone
- Plasma exchange: to remove disease-causing antibodies
What is used for maintenance of MS?
- Disease-modifying drugs- don’t really need to know them but just in case your feeling keen – thanks but im not xx
-
Beta-interferon: decreases the level of inflammatory cytokines
- Monoclonal antibodies e.g. alemtuzumab (anti-CD52) and natalizumab (anti-α4𝛃1-integrin)
- Glatiramer acetate: immunomodulator drug which acts as a ‘decoy’
- Fingolimod: a sphingosine-1-phosphate receptor modulator that keeps lymphocytes in lymph nodes so they can’t cause inflammation
What are some complications of MS?
- Genitourinary:urinary tract infections, urinary retention and incontinence
- Constipation
- Depression: offer mental health support if required
- Visual impairment
- Mobility impairment: offer physiotherapy, orthotics and other mobility aids
- Erectile dysfunction
What is Guillain-Barré syndrome?
An acute paralytic polyneuropathy. It is an autoimmune, rapidly progressive demyelinating condition of the peripheral nervous system
What are the risk factors for developing Guillain-Barré syndrome?
- Male
- Age 15-35 and 50-75
- Malignancies
- Vaccines (flu)
- Infections
What are the most common infections that trigger Guillain-Barré syndrome?
- Campylobacter jejuni (most common)
- Cytomegalovirus
- EBV
What causes Guillain-Barré syndrome?
- A pathogenic antigen resembles myelin gangliosides in the peripheral nervous system.
- The immune system targets the antigen and attacks the myelin sheath of sensory and motor neurones
- It occurs in patches along the length of the axon so is called segmental demyelination
What antibodies are found in 25% of people with Guillain-Barré syndrome?
- Anti-ganglioside antibodies (anti-GMI)
Describe the disease course of Guillain-Barré syndrome?
Symptoms usually start within 4 weeks of the preceding infection. The symptoms typically start in the feet and progresses upward.
Symptoms peak within 2-4 weeks, then there is a recovery period that can last months to years.
What are the signs and symptoms of Guillain-Barré syndrome?
- Symmetrical ascending weakness (starting at feet and moving up the body)
- Reduced reflexes
- Loss of sensation and pain
- Cranial nerve involvement such as facial nerve weakness
- Autonomic features (sweating, raised pulse)
- Struggling to breathe
What is used to diagnose Guillain-Barré syndrome?
A clinical diagnosis that is evidenced by progressive weakness and hyporeflexia in the weaker limbs.
The Brighton criteria is used for diagnosis. (This does not include letting your manager go to Chelsea or selling all of your best players) (it may include being - at time of writing - 3 positions higher, 4 points better off and having 2 games in hand over Chelsea)
What are the differentials of Guillain-Barré syndrome?
- Myasthenia gravis
- Transverse myelitis
- Polymyositis
What is the treatment for Guillain-Barré syndrome?
- IV immunoglobulins IV IG
- Plasma exchange (alternative to IV IG)
- Venous thromboembolism prophylaxis (PE is the leading cause of death)
What is the prognosis for Guillain-Barré syndrome?
80% will fully recover
15% will be left with some neurological disability
5% will die
What is Parkinson’s disease (PD)?
A neurodegenerative disorder characterised by the loss of dopaminergic neurons within the substantia nigra pars compacta (SNPC) of the basal ganglia.
What are the risk factors for developing PD?
Age: prevalence is 1% in 60-70 and 3% in those above 80
Gender: men are 1.5 times more likely than females to develop PD
Family history
Describe the pathophysiology of PD
- In PD there is progressive loss of dopamine-producing neurons meaning there is a reduction in the amount of dopamine produced at the substantia nigra
- Loss of these neurons results in reduction in action of the direct pathway and a resultant increase in the antagonistic indirect pathway which has a restrictive action on movement. Therefore bradykinesia and rigidity are key symptoms
- There is also formation of protein clumps Lewy bodies
What are the 3 key presentations of PD?
- Bradykinesia
- Tremor
- Rigidity
PD symptoms usually start unilaterally and then become bilateral later in the disease course.
What symptoms would not be present in the early stages of PD?
- Incontinence
- Dementia
- Early falls
- Symmetry
Can be a sign of normal pressure hydrocephalus
What does the bradykinesia look like in PD?
- Handwriting gets smaller
- Only take small steps (shuffling gait)
- Difficulty initiating movement
- Difficulty turning around when standing
- Reduced facial movements and expressions
What does the tremor look like in PD?
- A unilateral resting tremor. Described as pill rolling tremor looks like they are rolling pill between thumb and finger
- The tremor is worse at resting and when they are distracted like using the other hand
Frequency of 4-6 times a second
What is the rigidity like in PD?
- If you take their hand and passively flex and extend their arm at the elbow you will feel tension in their arm that gives way to movement in small increments (little jerks)
- Described as cogwheel
What are some other symptoms of PD?
- Depression
- Sleep disturbance and insomnia no REM
- Loss of sense of smell
- Postural instability
- Cognitive impairment and memory problems
What are the differences between a PD tremor and a benign essential tremor?
- PD= asymmetrical BET= symmetrical
- PD= frequency= 4-6 BET= 5-8
- PD= worse at rest BET= better at rest
- PD= improves with intentional movement BET= worse
- PD= no change with alcohol BET= better with alcohol
What is used to treat a benign essential tremor?
- Beta blocker (propranolol)
- Primidone
What is used to diagnose PD?
PD is a clinical diagnosis and should be suspected in a patient with bradykinesia and at least one of the following:
- Tremor
- Rigidity
- Postural instability
What is the management for PD?
Motor symptoms not affecting quality of life:
A choice of one of the following:
Dopamine agonist(non-ergot derived)
- Pramipexole, ropinirole
Monoamine oxidase B inhibitor (MOA-B)
- Selegiline, rasagiline
- Stop breakdown of circulating dopamine
Motor symptoms affecting the quality of life:
- Synthetic dopamine levodopa given with a drug that stops it being broken down. These are peripheral decarboxylase inhibitors. Carbidopa and benserazide.
Co-benyldopa (levodopa and benserazide)
Co-careldopa (levodopa and carbidopa)
What is the prognosis for PD?
PD is a chronic and progressive condition with no cure.
Overall, life expectancy is reduced with the mortality being 2-5 times higher for those aged 70-89 years old. Also, the risk of dementia is up to 6 times higher in PD patients.
What is Huntington’s disease?
An autosomal dominant genetic neurodegenerative condition that causes a progressive a progressive deterioration in the nervous system.
What causes HD?
- It is a trinucleotide repeat disorder that involves a genetic mutation in the HTT gene on chromosome 4
- There is a repeat of CAG which codes for glutamine 36 times in a row so patients have 36 glutamine in a row on the Huntington protein
- These mutated proteins aggregate within neuronal cells of the caudate and putamen causing neuronal cell death. This leads to decreased ACh and GABA synthesis. This leads to dopamine increase leading to excessive movement
What are primary headaches and give some examples?
No underlying cause relevant to the headache:
- Migraine
- Cluster
- Tension
- (Trigeminal Neuralgia)
What are red flag associated symptoms of headaches?
- Fever, photophobia or neck stiffness (meningitis or encephalitis)
- New neurological defect (raised ICP/stroke)
- Visual disturbance (GCA/ acute closure glaucoma)
- Vomiting (raised ICP, brain abscess and CO poisoning)
What are the headache symptoms of a migraine?
Last between 4-72 hours:
- Pounding or throbbing in nature
- Usually unilateral (can be bilateral more common in children)
- Photophobia
- Phonophobia (loud noises)
- Aura
- Nausea and vomiting
What is the diagnostic criteria for migraines with aura?
At least two headaches filling criteria shown in picture
What is the diagnostic criteria for migraines without aura?
At least five headaches filling criteria shown in picture
Describe the normal physiology of a neuromuscular junction
- Axons of motor nerves are situated across a synapse from from the post-synaptic membrane on the muscle cell
- The axons release a neurotransmitter from the pre-synaptic membrane. This neurotransmitter is acetylcholine.
- ACh travels across the synapse and attaches to nicotinic receptors on the post-synaptic membrane stimulating muscle contraction
What are the two other antibodies that can cause MG and how do they do it?
- Muscle specific kinase (MuSK)
- low-density lipoprotein receptor-related protein 4 (LRP4).
They are both proteins that are important for making the acetylcholine receptor. These antibodies lead to inadequate acetylcholine receptors causing MG
What are the signs of MG?
- Proximal muscle weakness: often affecting the face and neck
- Ptosis (drooping eyelid)
- Complex ophthalmoplegia: cannot be isolated to one cranial nerve
- Head drop: a rare sign due to weakness of cervical extensor muscles
- Myasthenic snarl: a ‘snarling’ expression when attempting to smile
What drugs should be avoided in MG?
What causes Lambert-Eaton myasthenic syndrome?
- Typically occurs in patients with SCLC. It is a result of antibodies produced by the immune system against voltage gated calcium channels in SCLC but this also targets the pre-synaptic terminal
- These channels are responsible for assisting the release of ACh at the synapse
Where does the median nerve provide sensory innervation for in the hand?
The palmar aspects and full fingertips of the:
- Thumb
- Index and middle finger
- The lateral half of the ring finger
Note that the palmar cutaneous branch of the median nerve provides sensation to the palm. However, this branch originates before the carpal tunnel and does not travel through the carpal tunnel. Therefore, it is not affected by carpal tunnel syndrome.
Where does the median nerve provide motor function for in the hand?
The three thenar muscles which make up the muscular budge at the base of the thumb:
- Abductor pollicis brevis (thumb abduction)
- Opponens pollicis
- Flexor pollicis brevis (thumb flexion)
The other muscle that controls thumb movement is the adductor pollicis (thumb adduction). However, this is innervated by the ulnar nerve.
What is Phalen’s test?
- Involves fully flexing the wrist and holding it in this position. Often this is done by asking the patient to put the backs of their hands together in front of them with the wrists bent inwards at 90 degrees.
- The test is positive when this position triggers the sensory symptoms of carpal tunnel, with numbness and paraesthesia in the median nerve distribution.
What is Tinel’s test?
- Involves tapping the wrist at the location where the median nerve travels through the carpal tunnel. This is in the middle, at the point where the wrist meets the hand.
- The test is positive when this position triggers the sensory symptoms of carpal tunnel, with numbness and paraesthesia in the median nerve distribution.
What is the classical presentation of a radial nerve palsy?
Wrist drop
What is the classical presentation of an ulnar nerve palsy?
Claw hand (4th/5th fingers claw up)
