MedReg+1 Rohrer Neuro

Developing people for health and healthcare

Neurology

Dr Jonathan Rohrer

Developing people for

health and healthcare

•Epilepsy

• Management of convulsive status epilepticus

• Focal and nonconvulsive status epilepticus

•Headaches

• Headache history

• Evaluation of sudden, severe headache

•Weakness

• Evaluation of acute weakness

• GBS and transverse myelitis

Overview



• A 65-year-old man presents to A+E. He had been found unconscious at

home by his wife who called an ambulance. He had come round by the

time the ambulance arrived but was confused.

• On his way to hospital he had a tonic-clonic seizure, and this had been

going on for 3 or 4 minutes when he is brought in to resus.

• What are you going to do first?

Epilepsy case 1



• Despite your treatment he continues to have an ongoing seizure – this

has now been going on for 11 or 12 minutes.

• What are you going to do next?

Epilepsy case 1



STEP 1: benzodiazepine;

give if fitting for > 5

minutes

STEP 2: if no

response to step

1 WITHIN 10

minutes, give

stage 2 agent

and inform

ICU/anaesthetics

STEP 3: if no

response to step

2 within 30

minutes of

onset,

anaesthesia and

ICU admission

Management of convulsive status epilepticus

For the full protocol see: A protocol for the inhospital emergency drug management of convulsive status epilepticus in adults. Jones et al. Practical Neurology 2014l 14: 194-197.

1. IV lorazepam – usual dose

2 to 4mg (max 2mg/min); if

necessary repeat up to a

max dose of 0.1mg/kg

2. or IV diazepam – usual

dose 5-10mg, up to 20mg if

necessary; do not give too

fast to avoid respiratory

depression (max 5mg /min)

1. IV phenytoin – 18mg/kg;

max rate 50mg/min; into

large or central vein with

ECG/blood pressure

monitoring

2. Ensure ICU/anaesthetics

aware of patient

GENERAL MEASURES in parallel

1. Secure airway and resuscitate

2. Administer oxygen

3. Assess cardiorespiratory function

4. Establish IV access

5. Measure CBG and correct hypoglycaemia

6. Check temperature

7. Check blood gases

8. If poor nutrition/alcohol abuse suspected

give Pabrinex

9. Take blood for FBC, U+Es, LFTs, clotting,

glucose, Ca, Mg, CK, AED levels, tox screen



• He has now been intubated and ventilated and is being taken to ITU.

• What are you going to do next?

Epilepsy case 1



• Pre-existing epilepsy – concurrent illness, not taking AEDs etc.

• Metabolic disturbance – electrolyte abnormalities, hypoglycaemia, renal

failure

• CNS infection – meningitis, encephalitis

• Stroke

• Head trauma

• Drugs or alcohol

• Hypoxia/cardiac arrest

• Brain tumour or other SOL

• Hypertensive encephalopathy/PRES

• Autoimmune encephalitis e.g. anti-VGKC, anti-NMDA antibodies

Epilepsy case 1 – why is this person in SE?



• 36 year old man with known Sturge-Weber syndrome attends A+E. He

has known epilepsy and is on carbamazepine 300mg BD.

• He has had continuous seizures for the last 30 minutes which are focal,

affecting the right arm and leg only and in full consciousness.

• He has been given 4mg of lorazepam and loaded with phenytoin but

they are still ongoing – what would you do?

Epilepsy case 2



• Continuous focal motor seizures (epilepsia partialis continua) can be

difficult to treat

• Avoid sedative and anaesthetic agents if possible

• Next steps – options include:

• IV levetiracetam 30mg/kg over 10 minutes

• IV valproate 30mg/kg over 5 minutes

Epilepsy case 2



• A 32-year-old woman presents to A+E with a sudden, severe headache.

It started 4 hours ago and her family say she has been a bit confused

since. She says that she feels nauseous.

• What will you ask her and what would you do next?

Headache case 1



• History of the headache itself including time to peak intensity and

duration. Are they someone who has headaches usually? How many a

month/year usually?

• Meningitis (if acute): neck stiffness, fever, rash, photophobia

• Migraine: unilateral or bilateral; nausea/vomiting, photophobia,

phonophobia, osmophobia, movement sensitivity, aura

• Trigeminal autonomic cephalgias (SUNCT 5s-4m – paroxysmal

hemicrania 2-30m – cluster headache 15m-3h): unilateral; red eye,

tearing, rhinorrhoea, nasal congestion, ptosis, miosis, restlessness

• Pressure-related headache: time of day, effect of posture, effect of

Valsalva manoeuvres, visual obscurations

• Temporal arteritis: jaw claudication, scalp tenderness/sensitivity

• Focal neurological symptoms

The headache history



• Usually fit and well. Not on any medication apart from OCP.

• On examination she has a normal exam with no focal neurology. She

knows where she is and what day it is.

• She has a normal CT head and goes on to have a lumbar puncture.

This shows an opening pressure of 32cmH2O with a normal white cell

count, normal protein and normal glucose.

• What would you do next?

Headache case 1



What causes acute severe headache?



Primary headaches

• Migraine

• Cluster headache and other trigeminal autonomic cephalalgias

• Others e.g. primary thunderclap headache

Secondary headaches

• Head or neck trauma

• Cranial or cervical vascular disorder: SAH, ICH, ischaemic stroke, dissection,

venous sinus thrombosis

• Nonvascular intracranial disorder: raised or low intracranial pressure, tumour,

pituitary apoplexy

• Due to a substance or its withdrawal

• Infection: intracranial or systemic

• Due to problems in the head, neck and cranial structures: acute glaucoma

What causes acute severe headache?



If meningitis suspected,

investigate and treat

accordingly

Ask, is time to peak intensity

<5 minutes and headache

duration >1 hour

If yes, strongly

consider SAH and

organise CT head.

If normal then

perform LP >12

hours after onset

with OP, cell count,

glucose, protein,

spectrophotometry

If no, but warning

features present

(see below) then

CT head/discuss

with neurology

team

Emergency evaluation of sudden, severe headache

MAIN WARNING FEATURES

• New onset or change in headache in people

over 50

• Time to peak intensity of <5 minutes

• Focal neurological symptoms

• Non-focal neurological symptoms e.g. seizure

or cognitive disturbance

• Change in headache frequency, characteristics

or associated symptoms

• Abnormal neurological exam

ADDITIONAL WARNING FEATURES

• Headaches that change with posture

• Headaches waking the patient up, or

precipitated by Valsalva manoeuvres

• Risk factors for cerebral venous thrombosis

• Jaw claudication or visual disturbance

• Neck stiffness

• Fever and rash

• New onset headache in patient with HIV

• New onset headache in patient with cancer



Weakness



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Where? (Anatomy)



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Where? (Anatomy)

What? (Pathology)



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Spine Brain

In

the

UMN

Question 1

Is it a

hemiparesis,

quadraparesis

or

paraparesis?

HE

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the

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Question 2

What are the

sensory

features?HE

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the

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Question 3

Are there any

cranial nerve

signs?HE

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Beyond

the

UMN

Question 1

Is weakness

symmetrical or

asymmetrical?

Asymmetrical/unilateral Symmetrical



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Question 2

If symmetrical,

is it distal or

proximal?

DIS

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Symmetrical



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Question 3

If

asymmetrical,

what is

sensory

impairment?

Asymmetrical/unilateral

NO

RM

AL

DE

RM

AT

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A

L

DE

RM

AT

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A

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NE

RV

E



DERMATOMAL NERVE



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NM

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s

Beyond

the

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The

example of

foot drop

NO

RM

AL

DE

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AT

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A

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AT

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A

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MNDNormal

sensation



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Nerve Nerve

s

Beyond

the

UMN

The

example of

foot drop

NO

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AL

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A

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L5 radiculopath

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Beyond

the

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The

example of

foot drop

NO

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AL

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AT

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A

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Lumbar

plexopath

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example of

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Peronea

l nerve



• A 54-year-old man presented to A+E with a three day history of difficulty

walking and tingling in his legs. This initially started in his feet but had

now progressed to affect the whole of both lower legs. He had come

today as he had also developed difficulty passing urine and hadn’t been

for six hours. He had not long got back from a holiday in India.

• On examination he had a normal cranial nerve territory and upper limb

examination but in the lower limb he had decreased tone with weakness

in the hip flexors and the ankle dorsiflexors bilaterally. Reflexes were

present and symmetrical with downgoing plantars. Sensation was

decreased to pinprick throughout the legs.

• What would you do next?

Weakness case 1



GBS vs transverse myelitis

Motor

Sensory

Autonomic

CN

Ix

Ascending weakness;

become areflexic but can be

intact initially

Transverse myelitis

May be minimal on exam

but can be ascending

Cardiovascular >

bladder/bowel early

May have facial or EOM

weakness

CSF: elevated protein but

not WCC

EMG/NCS: demyelination

GBS

Para or quadraparesis;

reflexes usually brisk

Spinal cord level usually

Early loss of bladder/bowel

control

None

CSF: may have increased

WCC/protein

MRI: usually abnormal



Please email me if any questions or you want any references:

[email protected]



Some brainstem anatomy

MIDBRAIN

PONS

MEDULLA




1. Rule of 4MIDBRAIN

PONS

MEDULLA





PONS

MEDULLA

3

4





PONS

MEDULLA

3

4

65

7

8





PONS

MEDULLA

3

4

6

12

5

7

8

9

10

11




1. Rule of 4

1 provisoMIDBRAIN

PONS

MEDULLA

3

4

6

12

5

7

8

9

10

11




1. Rule of 4

1 proviso

2. Rule of 12

MIDBRAIN

PONS

MEDULLA

3

4

6

12

5

7

8

9

10

11

LATERAL MEDIAL




1. Rule of 4

1 proviso

2. Rule of 12

3. Rule of S+M

Lateral =

sensory and

sympathetic

Medial = motor

MIDBRAIN

PONS

MEDULLA

3

4

6

12

5

7

8

9

10

11

LATERAL MEDIAL



Where is the brainstem syndrome?

• Left facial sensation loss, left face weakness, left hearing lossand right arm and leg sensory loss





• Left lateral pons






• Tongue deviation to the right and left hemiparesis






• Tongue deviation to the right and left hemiparesis

• Right medial medulla

Documents

MedReg+1 Rohrer Neuro