Neuro assessment and neurosurgery Flashcards by Emily Roberts

What is core in the neurological examination and why?

General appearance
Vital signs
Gait
Fundoscopy (papilloedema/optic atrophy)
UMN signs
Vibration sense
Patient cannot tell you they've lost these

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What do you do for a patient that cannot give you a history?

ABC rescuscitation
Collateral history - who it is gives more weight
Generalised appearance
Vital signs - temp, pulse rate, resp rate, BP ,sats
Mini-neurological examination

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What is in a mini-neurological examination?

Pupils
GCS
Lateralising signs

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Why might you get fixed dilated pupils?

CN III palsy
Travels over petrous part of temporal bone containing inner and middle ear structures (parasympathetic fibres)
Being pushed down onto bone
Bad sign
Check not blind in one eye - should still get indirect light response if normal and blind in eye

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What should you ask about in a neurological history to help improve QOL?

Mobility
Eating/drinking/nutrition
Communication
Personal hygiene/continence
Interpersonal relationships - psychological disorder underlying
School/job/hobbies
Sleep

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What 2 syndromes do signs appear before symptoms and why is this important to know?

Diabetic peripheral neuropathy
Cord compression in neck
Screen for these issues

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What is the pain tool?

Site
Radiation
Onset
Precipitating factor
Duration
Course
Progression
Character
Severity
Disturbing sleep
Alleviating/exacerbating factors
Associated symptoms
Ever had before
Response to conservative measures
Significantly interfering with lifestyle
- Mobility
- Communication
- Interpersonal relationships
- School, work and/or hobbies
- Continence, sexual function, and personal hygiene
- Sleep
- Eating/drinking/nutrition

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What is a clinical syndrome?

Cluster of symptoms and signs

Most have underlying structural abnormalities

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What are the S&S of myopathies?

Hair, stairs, chair - difficulty getting out of chair, difficulty walking up stairs, difficulty washing hair
Ask them to squat using one leg
Muscular dystrophies

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What are the S&S of myasthenic syndromes?

Fatigueable, repeatable activity
Blink can fatigue
Walking can be difficult
Listening to story to know at what point sign might be positive eg walking distance
MG - most common
Lambert Eaton syndrome (paraneoplastic)

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What are the main mononeuropathies?

Carpel tunnel syndrome and ulnar nerve entrapment at elbow
Radial nerve injury - fracture of humerus
Axillary nerve injury - shoulder dislocation/injury

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What are the S&S of mononeuropathies?

Pain/paraesthesia/numbness
In nerve distributions
Generally affect upper limb those affecting lower limb are rare
Have no signs
Investigated with EMG/NCS

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What are the S&S of peripheral neuropathies?

Paraesthesia
Numbness/loss of sensation
Diabetes - risk factor

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What are the S&S of vertebral pain syndrome?

Localised aching pain, limited radiation, stiffness/restriction of movement
Worse with activity and absence of associated neurological symptoms
Visible/palpable paravertebral muscle spasm, paravertebral tenderness and restriction on movement on examination
Commonly wear and tear/degenerative changes rarely - TB, bacterial discitis, osteomyelitis, osteoporotic fractures, metastatic disease (particularly if thoracic)

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What are the S&S of radiculopathy?

Often radiating limb pain, in pattern of dermatome, sharp/shooting in character, only a small portion have associated neurological symptoms - dermatomal sensory loss, less commonly myotomal muscle weakness

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What will you lose in a C6 radicuolpathy?

Thumb dermatome
Biceps myotome
Biceps jerk

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What will you lose in a C7 radiculopathy?

Middle finger dermatome
Biceps myotome
Triceps jerk

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What will you lose in an L5 radiculopathy?

Dorsum of foot/big toe dermatome, dorsiflexion (standing on heels)

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What will you lose in a S1 radicuopathy?

Ankle, lateral aspect of foot/sole of foot/little toe dermatome
Plantar flexion (standing on toes)
Ankle jerk

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What is spinal claudication?

Radiculopathic syndrome

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What are the S&S of spinal claudication?

Bilateral radiating leg pain/paraesthesia that comes on with walking and have to stop and rest for a number of minutes before walking on again (walking distance limited)
Symptoms relived by leaning forwards

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What are the red flag symptoms in radiculopathy?

Constant bilateral radiating leg pain
Perineal numbness
Foot weakness
Urinary symptoms of immediate concern

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What are the S&S of myotomal disorders?

Neuroclinical syndrome involving spinal cord
Commonest cause - disc-osteophyte cord compression
If left too long, not likely to make significant recovery
Signs before symptoms - test for long tract signs

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What are the S&S of RIP?

Gradual onset, progressive headache, val salva component - worse on coughing and straining
Associated with N&V, double vision, general deterioration with respect to cognitive functioning and mobility
Present with deteriorating level of consciousness
Look for drowsiness, papilloedema, paralytic squint (3rd/4th/6th nerve palsy)
Fixed dilated pupil
Reduced level of consciousness

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What are the S&S of meningeal irritation?

Severe headache, vomiting, photophobia, neck stiffness
Sudden onset if SAH
Drowsy, pyrexia if meningitis, photophobic, neck stiffness
CT then LP

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How can you differentiate between acute confusional state and dementia?

Duration of confusion
Acute - secondary brain problem
Dementia - primary brain problem

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How does cerebellar syndrome present?

Feels drunk
S&S are ipsilateral to side of lesion
Signs - gait ataxia, ataxia on finger to nose testing, nystagmus

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How do frontal lesions present?

Contralateral limb weakness
Motor dysphasia for dominant frontal lobe
Personality in anterior frontal love duplicated so only affected if both sides affected

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How do parietal lesions present?

Non-dominant - contralateral sensory disturbance (no limb pain)
Dominant - as per non-dominant with higher sensory processing associated issues such as dylexia, dysgraphia, dyscalculia and astereognosis

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How do temporal lesions present?

Dominant - understanding of speech and memory

Non-dominant - no clinical syndrome

How do occipital lesions present?

Contralateral visual field issues

How do you measure cerebral perfusion pressure?

CPP = MAP - ICP
MAP - mean arterial pressure
CPP should be 60-70mmHg
- Below = brain hypoperfusion and contributes to secondary brain injury
- Above in context of brain injury where impaired cerebral vasculature = exacerbations of brain oedema and contributes to secondary brain injury

What does the intracranial pressure volume curve show?

Pressure controlled for some time due to compensation when volume increases
After certain volume, small increase in volume will cause marked increased in ICP

How do you manage a seizure?

Time the seizure
Insert nasopharyngeal airway in nostril and provide supplemental O2 by mask
IV access
Attach O2 sats monitor and watch for hypoxia whilst appropriately managing airway
Only administer IV benzodiazepine if > 10 mins as risk of respiratory suppression leading to unnecessary intubation/ventilation (IV midazolam as short-acting)
Loading dose of phenytoin/valproate/levetiracetam IV (1g) as infusion over 15 mins whilst cardiac monitoring
Write up maintenance if not on regular anti-convulsant
Once passed, send U&E blood test screening for electrolyte disturbance and consider CT
Possibility of peri-ictal aspiration of secretions or vomit with risk of subsequent lower respiratory tract infection considered

What is mannitol and what dose should you use?

Osmotic diuretic, used as short-term measure to buy time in situation of acutely rising ICP
100ml of 10% mannitol or 50ml of 20%

What is hydrocortisone cover and when should you use it?

If on longterm corticosteroids or where any doubt about hypopituitarism or adrenal suppression in neuro-critical care context or peri-operatively cover with hydrocortisone 100mg QDS IV with subsequent dose reduction over number of days as per endocrinologist advice

When do you use dexamethasone? What is the dose?

Given peri-operatively for patients undergoing surgery for intracranial tumours
Dose 4mg QDS or 8mg BD with dose reduction over days Not continued beyond 2 weeks due to risk of adrenal suppression or Cushing’s
Daily glucometer readings in case of hyperglycaemia
Watch out for steroid psychosis

What is important about antiplatelets and anticoagulation with neurosurgery?

Significant risk factors for acute intracranial haemorrhage, both traumatic and spontaneous
When acute neurosurgical pathway identified then stop agents and effects reversed as matter of urgency with consultation with haematologist
Restart on instruction of surgeon

How do you manage diabetes insipidus?

Initial management maintain robust fluid balance chart allowing patient to drink to thirst then consider desmopressin
Involve endocrinologist

How do you manage hyponatraemia?

Most commonly cerebral salt wasting in neurosurgical patients
Less commonly SIADH
Initial management salt supplements, volume IV crystalloid and consideration of mineralocorticoid (involve endocrinologist)
SIADH - fluid restriction, endocrinologist involvement

How do you manage neuropathic pain?

Gabapentin and pregabalin - radicular pain
Carbamazepine - trigeminal neuralgia can use with anti-depressants
Topirimate - chronic refractive head pain
Dose regimens, S/E, and blood monitoring as per BNF
Need to be taken for at least 2 weeks before judging benefit
For women of childbearing age - appropriate advice needs to be given concerning contraception due to small teratogenic risk

When should you intubate/ventilate someone?

Agitated and CNS imaging required
In circumstances of acute neurologic deterioration
Persisting poor level of consciousness
Where patient at risk of or has respiratory failure and requires ventilatory support
Status epilepticus
Significant intra-operative brain swelling noted

What happens when someone is sedated and what should you therefore do beforehand?

Sedating and paralysing agent required

Pre-intubation GCS and lateralising sign assessment documented immediately before administration of agents

How common are neurosurgical problems?

SAH incidence 10-20/100,000 per year
Primary brain tumours 10-20/100,000 per year but increasing discovery of small incidental benign meningiomas due to better access to MRI so true incidence likely higher
Secondary brain tumours occur in 20% of patients dying of cancer
Trauma commonest cause of death in children and young adults with head injury being commonest mode of death
Brain tumours second commonest cause of cancer in children after leukaemias
Spinal degenerative disease is commonest time of work in Western World

How common are head injuries?

Minor head injuries 95% patients attending hospital with head injury
Commonest cause of death and disability in people aged 1-40
For minor - appropriate discharge advice including written instructions and contact details should be provided to patient and next of kin

How do you assess someone with a head injury?

Assess within 15 minutes of arrival in A&E
ATLS principles even for minor head injuries
ABCDE
Ongoing assessment schedule for performing vital signs and mini-neurological obs if not intubated/ventilated
Intubated/ventilated - immediate pre-intubation assessment of GCS and lateralising signs
Low threshold to consider possibility of co-existing cervical spine injury
Only ascribe depressed level of conscious to intoxication after significant brain injury excluded
Suture any scalp laceration before moving patient out of A&E as can die of blood loss from scalp wound
Do not move patient out of A&E resus area until vital signs are normal

When should you do a CT head? What are the indications?

Usually within 1 hour of arrival
Indications
- Reduced GCS on admission or GCS that subsequently reduces
- Severe headaches
- Drowsiness
- LOC or amnesia > 5 mins
- More than 1 episode of vomiting
- Children < 1 with craniofacial bruising, swelling, significant scalp laceration > 5cm
- Any suspicion of non-accidental injury in child
- Sign of basal skull fracture
- Focal neurologic deficit
- Scalp laceration with palpable fracture within laceration
- Skull indentation suggestive of closed depressed skull fracture
- Returning within 48 hrs of A&E
- Dangerous mechanism of injury
- Bleeding diathesis including coagulopathy in context of large volume blood loss or on medication such as warfarin
- Seizure
- Where assessment is difficult
- Where multiple trauma patient without apparent head injury likely to have extended period anaesthetic for emergency surgery

When should you involve neurosurgery with a head injury?

All patients with non-minor head injury discussed with neurosurgeon following CT scan of head
Severe head injuries managed in specialist centres with immediate access to neurosurgery
Severe head injury - persistent impaired level of consciousness post-resus, focal deficit, seizure, CSF leakage, definite or suspected penetrating head injury, significant positive finding on CT

What do you need to know on a neurosurgery referral?

Make sure seen patient, read notes, and have CT head scan results up
Requested CT radiographer to immediately image-linked patients imaging to neurosurgical centre if not part of hospital system
Know mechanism of injury, estimated time, relevant background history
Know current vital signs
Be able to give current mini-neurological examination findings or immediate pre-intubation mini-neurological examination findings and current pupillary status
Be able to list any other injuries identified, any resuscitative interventions, and what other imaging done
Will not accept if not safe to transfer

What is important to know for legal aspects of head injuries?

Often sustain injuries in circumstances that may lead to investigations
Death from head injury notifiable to coroner
Important to
- Keep good medical notes including documenting timing of notes entries
- Shave whole head of patient and draw or photography extent of injuries
- Ensure that police are aware of facts of situation so that forensic evidence not lost
- Ensure follow any rules concerning collecting and labelling of evidence
- Send toxicology screen
- Safeguarding for children

What are the different types of brain injury?

Systemic (early) brain injury
Primary
Chronic subdural haematoma
Late secondary brain injury

What is a systemic (early) brain injury?

Hence why ABC before D is important

Patient will die from blocked airway before head injury

What is are the 2 types of primary brain injury?

Minor

Serious

What are the types of serious brain injury?

Severe closed head injury - may be intubated/ventilated, ICP monitoring and management, minimise brain swelling but may require decompressive craniectomy
Compound depressed skull fracture - require neurosurgery to clean wound, reconstruct skull, and close and dura and scalp defects, IV antibiotics for 3 days
Penetrating injury - never remove object
Gun shot injuries - surgery usually required, prognosis poor for high velocity compared to low due to cavitation
Intracranial haematoma - subdural and extradural usually require emergency evacuation via craniotomy

What is a chronic subdural haematoma?

Generally seen in older population
Over time goes through degradative process, liquifies and expands to cause significant mass effect
Predisposing factors - aspirin, anticoagulation
Clinical syndrome presentation - acute confusional state, lobe syndrome, and/or raised ICP, CT head
Burrhole drainage
Recurrence over subsequent weeks requiring redrainage occurs in up to 10%

What is a late secondary brain injury?

Brain swelling
Delayed hydrocephalus
CNS infection
Post-operative haematoma
Systemic infection eg pneumonia

How do intracranial tumours present? How are the diagnosed?

Seizures, raised ICP, intracranial localising syndromes
Dementia, acute confusional state, stroke and one or more cranial neuropathies
Cranial imaging - CT head then MRI
Can be found incidentally

What are the different types of intracranial tumours?

Secondary
Primary
- Parenchymal/intrinsic
- Extra-axial/extrinsic

What are parenchymal intracranial tumours?

2/3rds primary
Arise from brain substance and generally merge in indistinct manner with normal brain tissue
Gliomas
Glioblastoma multiforme grade 4, don’t met outside CNS
WHO grading 1-4

What are atra-axial intracranial tumours?

1/3
Arise from structure outside brain parenchyma itself, indent and surgically separable from brain
2-3 mm increase in cross-sectional diameter per year
If benign - long term surveillance scanning with treatment in small proportion
Meningiomas
Pituitary adenomas
Schwannomas

How are brain tumours treated?

Interval imaging usually MRI
Surgery for symptoms management, prevent likely function or life-threatening deterioration, or for diagnostic uncertainty
Craniotomy
May be incomplete removal
Radiation - radiotherapy of whole brain (primary) or stereotatic radiotherapy (secondary)
Chemotherapy - temozolamide

Why might ischaemic strokes be under neurosurgery?

Come to surgery for decompression - small minority if swelling causing raised ICP
For cerebellar infection as posterior fossa tighter box
For infarction in territory of MCA
Carotid endarterectomy

How do spontaneous brain parenchymal haemorrhages present?

Supratentorial - lobe syndrome, meningeal irritation, raised ICP
Infratentorial - cerebellar syndrome, meningeal irritation, raised ICP

How are spontaneous brain parenchymal haemorrhages treated?

CT scan
Reverse anticoags
Control hypertension in critical care with IV labetalol and monitoring
Discuss with neurosurgeon if clinical status flexing or better
Indication - deteriorating consciousness
Consideration of an underlying cause

What can cause SAH?

Intracranial berry aneurysms (80-90%)
- 1/3 die immediately
- 1/3 die in next 48 hrs
- 1/3 survive of which 10% suffer stroke from SAH associated arterial vasospasm
Rare causes - arteriovenous malformation, arterial dissection, tumour
Cause undetermined

How can you treat SAH?

Management - deal with complication of aneurysmal SAH and secure causative berry aneurysm at appropriate time point
Secure intracranial berry aneurysm

What are the complications of SAH?

Hydrocephalus requiring insertion of external ventricular drain
Aneurysm associated haematoma requiring craniotomy and evacuation
Hyponatraemia
Vasospasm leading to infarction, nimodipine given pre-emptively
LRTI

What are the types of spinal degenerative disease?

Vertebral pain syndrome, radiculopathy and myelopathy

Hard disc osteophyte formation or soft disc prolapse

How is spinal degenerative disease diagnosed?

Spinal imaging, CT myelogram if MRI CI

What is myelopathy and how is it treated?

Disc osteophyte compression of cervical cord manifested by possible symptoms, presence of one or more long-tract signs, imaging demonstrated canal stenosis with overt cord compression requires surgical decompression
Fast-tracked

What is vertebral pain syndrome and how is it treated?

No benefit from surgery for neck/shoulder or low back/buttock
Advised on conservative pain management

What is radiculopathy and how is it treated?

For severe constant persistent and refractive radicular pain
Relief of pain 80-90%
Doesn’t benefit numbness/sensory loss or muscle weakness
Should have trialled neurotropic agents
Complete L5/S1 radiculopathy secondary to disc prolapse refer to on-call neurosurgery
Cauda equina emergency

What are the potential complications of neurosurgery?

Haemorrhage/intracranial haematoma
Hydrocephalus
Hypercapnia (ABG) 
Hypoxia (ABG) - LRTI/PE
Hyponatraemia (U&E) - cerebral salt wasting/SiADH
Infarct 
Infection 
Seizures
Swelling of brain

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Neuro assessment and neurosurgery Flashcards

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