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3a > Neuro > Flashcards

Neuro Flashcards

1
Q

Which dermatomes supply which areas of the arm?

A 
C5 = just below shoulder
C6 = radial forearm. thumb and first finger
C7 = middle two digits 
C8 = little finger and part of ulnar forearm
T1 = ulnar top part of arm
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2
Q

Which lumbar root controls the ankle jerk reflex?

A

S1

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3
Q

Which cervical roots control the biceps and triceps reflexes?

A

C6 and C7

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4
Q

What happens in Brown Sequard syndrome?

A

A hemisection of the spinal cord occurs causing ipsilateral loss of proprioception, fine touch and motor function and contralateral loss of pain and temperature

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5
Q

Name 2 ascending spinal tracts and their functions

A

Spinothalamic = pain and temp laterally and crude touch and pressure anteriorly
Dorsal column medial lemniscus (DCML) = proprioception, fine touch and vibration

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6
Q

Name 2 descending spinal tracts and their functions

A 
Corticospinal = motor control of skeletal body muscles 
Corticobulbar = motor control of head and neck muscles
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7
Q

Which spinal tracts are affected in Brown Sequard syndrome?

A

DCML (proprioception and fine touch) and Corticospinal (motor function) which decussate in brain
Spinothalamic = pain, temp, crude touch and pressure which decussates in spinal cord so causes contralateral symptoms

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8
Q

List the symptoms that cerebellar dysfunction causes

A 
D-ysdiadochokinesia
A-taxia
N-ystagmus
I-ntention tremor
S-lurred speech
H-ypotonia
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9
Q

What are the 3 layers of the meninges (from outer to inner)?

A

Dura mater
Arachnoid mater
Pia mater

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10
Q

Where is CSF contained?

A

The sub arachnoid space

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11
Q

How does CSF re enter circulation

A

Arachnoid granulations into the dura allow it to re enter circulation via the dural venous sinuses

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12
Q

Describe the pathway of vessels in the circle of willis from bottom to top

A

Basilar artery (pontine arteries coming off)
Superior cerebellar artery
Posterior cerebral artery
Posterior communicating artery
Middle cerebral artery feeding into internal carotid
Anterior communicating artery
Anterior cerebral artery

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13
Q

Which foramina do the 1st and 2nd CNs leave by?

A

Cribriform plate = olfactory

Optic canal = optic nerve

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14
Q

Which CNs leave the brain via the superior orbital fissure?

A

Oculomotor (3)
Trochlear (4)
Ophthalmic (5)
Abducens (6)

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15
Q

Which foramina do the mandibular and maxillary CNs leave by?

A 
Maxillary = foramen rotundum
Mandibular = foramen ovale
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16
Q

Which CNs leave via the internal acoustic meatus?

A

Facial (7) and vestibulocochlear (8)

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17
Q

Which foramina do the glosopharyngeal, vagus and accessory CN leave by?

A

Jugular foramen

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18
Q

Which foramina does the hypoglossal CN leave by?

A

Hypoglossal canal

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19
Q

Name some structures that make up the basal ganglia

A

Caudate nucleus, Lentiform nucleus (putamen and globus pallidus), claustrum, subthalamic nucleus and substantia nigra

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20
Q

What is the role of glial cells?

A

Support, nourish and insulate neurones by removing waste products of metabolism

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21
Q

Give 4 example of glial cells

A

Astrocytes, oligodendrocytes, microglia and ependymal cells

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22
Q

What is CSF produced by?

A

Choroid plexus which covers both the lateral ventricles and the roof of the 3rd and 4th ventricles

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23
Q

Give 4 roles of CSF

A

Buoyancy, protection, homeostasis and clearing waste

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24
Q

What are some UMN signs?

A

Hypertonia, hyperreflexia, weakness/paralysis, spasticity and clonus

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25
Q

What are LMN signs?

A

Hypotonia, hyporeflexia, flaccid muscle weakness or paralysis, fasciculations and muscle atrophy

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26
Q

What causes Horners syndrome?

A

A lesion of the sympathetic chain supplying the eye

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27
Q

What triad of symptoms is Horner syndrome characterised by?

A

Ptosis (drooping of eyelid)
Anhidrosis (lack of sweating)
Miosis (constricted pupil on ipsilateral side)

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28
Q

What is MS?

A

A chronic inflammatory autoimmune disorder of the CNS causing multiple areas of demyelination within the brain and spinal cord (oligodendrocytes are targeted)

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29
Q

What are the patterns of MS?

A 
Relapsing remitting (80%) symptoms come and go
Secondary progressive following on from relapsing remitting 
Primary progressive (10-15%)
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30
Q

State some signs and symptoms of MS

A

Limb numbness, tingling and weakness
Visual = unilateral optic neuritis (acute pain in eye on movement), blurred vision or hemianopia
Brainstem demyelination = diplopia, vertigo, dysphagia or nystagmus
Autonomic symptoms = bladder symptoms, sexual dysfunction and loss of thermoregulation
Lhermittes sign = tingling electric shock shooting up spine
Uhthoffs phenomenon = symptoms worse in heat

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31
Q

What is the key diagnostic criteria of MS?

A

Lesions must be disseminated in both time and space

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32
Q

What is the management of MS?

A

Acute relapse = steroids eg IV methylprednisolone

Frequent relapse = sc interferon beta, monoclonal abs, physio, muscle relaxants

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33
Q

What are the 2 types of stroke (CVA) and state causes of both

A

Ischaemic (85%) = small vessel occlusion, cardiac emboli eg due to AF, vasculitis
Haemorrhagic (15%) = trauma, aneurysm rupture, thrombolysis, SAH

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34
Q

What are common symptoms of an ACA stroke?

A

Leg weakness and sensory disturbance
Gait apraxia
Incontinence
Drowsiness

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35
Q

What are common symptoms of an MCA stroke?

A

Contralateral hemiplegia (more in arms)
Contralateral sensory loss
Hemianopia
Dysphasia

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36
Q

State some symptoms that may occur in a posterior circulation stroke

A 
Very catastrophic
Motor deficits eg weakness, clumsiness and paralysis
Dysphagia 
Visual disturbances
Altered consciousness
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37
Q

What are lacunar infarcts and what symptoms do they cause?

A

Small infarcts around the midbrain and internal capsule eg basal ganglia, thalamus and pons and cause pure motor or sensory signs

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38
Q

What is the management for an ischaemic stroke?

A

Thrombolysis within 4.5 hours of symptom onset
Give tissue plasminogen activator eg Alteplase
Start antiplatelet therapy eg Clopidogrel after

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39
Q

What is the management for a haemorrhagic stroke?

A

Control hypertension,
Frequent GCS monitoring
May need surgery

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40
Q

What are the most common type of primary brain tumours?

A

Gliomas (glial cell in origin) eg astrocytoma

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41
Q

Why are brain tumours not truly differentiated as benign or malignant?

A

All tumours even “benign” ones cause significant morbidity and mortality as are space occupying and increase the ICP

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42
Q

What are the 4 main symptoms of brain tumours?

A

Symptoms of raised ICP eg progressive headache, drowsiness, papilloedema (swelling of optic disc)
Progressive neurological deficit depending on area affected
Seizures
Lethargy/tiredness

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43
Q

What are the most common neoplasms that metastasise to the brain?

A 
Non small cell lung cancer
Small cell lung cancer
Breast
Melanoma
Renal cell 
GI
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44
Q

What is charcot marie tooth syndrome?

A

A group of inherited peripheral neuropathies causing muscle weakness starting from feet, sensory loss and spinal deformities

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45
Q

What are the main causes of bacterial meningitis in adults and children?

A

Streptococcus pneumoniae
Haemophilus influenzae
Neisseria meningitidis

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46
Q

What are common causes of viral meningitis?

A

EBV
Mumps
Herpes simplex
HIV

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47
Q

What are risk factors of meningitis?

A

Intrathecal drug administration, immunocompromised, crowding, IVDU, malignancy and diabetes

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48
Q

What are signs and symptoms of bacterial meningitis?

A

Non specific features eg fever, vomiting, rigors, headache, lethargy
Photophobia
Stiff neck
Meningococcal septicaemia = a non blanching petechial rash
Positive kernigs sign (resistance on passive knee extension when hips fully flexed)
Positive brudzinkis sign (hips flex on bending head forward)

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49
Q

How is bacterial meningitis diagnosed?

A

Blood cultures to see if septicaemia is present

Lumbar puncture at L4 and CSF microscopy (give empirical abs if not done within 30 mins)

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50
Q

How is bacterial meningitis managed?

A

IV Ceftriaxone is initial treatment because is broad spectrum and crosses the BBB
If >50/immunocompromised add Amoxicillin to cover listeria

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51
Q

What further actions do you need to take if it is found that the cause of meningitis is N meningitidis?

A

Alert public health and give prophylaxis to close contacts - Rifampicin or Ciprofloxacin to eradicate nasopharyngeal carriage of the organism

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52
Q

What is encephalitis?

A

Inflammation of the brain parenchyma

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53
Q

What causes encephalitis?

A

Mainly viral causes eg Herpes simplex, mumps, HIV

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54
Q

How does encephalitis present?

A

Triad of fever, headache and altered GCS
May begin with prodrome phase = flu like illness then is acute rapid development of altered consciousness with confusion, drowsiness, coma and seizure
May have signs of meningitis eg fever, headache and neck stiffness

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55
Q

How is encephalitis managed?

A

Give antivirals eg Acyclovir to cover herpes simplex

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56
Q

What is the pathophysiology of herpes zoster (shingles)?

A

It affects the peripheral nerves
If reactivated in the dorsal root ganglion it travels down the affected nerve via the sensory root in dermatomal distribution

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57
Q

How does Herpes Zoster present?

A

Pre eruptive = pain and paraesthesia in a dermatomal distribution and may feel generally unwell
Eruptive phase = rash appears consisting of papules and vesicles, neuritic pain

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58
Q

What is the management of Herpes Zoster?

A

Oral antiviral therapy within 72 hours of rash eg Acyclovir

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59
Q

Name some types of dementia

A 
Alzheimers disease
Vascular dementia
Lewy body dementia
Fronto temporal dementia
Parkinsons
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60
Q

How does Alzheimers disease present?

A

Insidious onset with steady progression
STM loss is most prominent early symptom
Slow disintegration of personality, intellect, language and visuospatial skills

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61
Q

How does Vascular dementia present?

A

Stepwise deterioration

History of TIAs or strokes

62
Q

How does dementia with lewy bodies present?

A

Fluctuating cognition
Impairment in attention or cognition before memory loss
Visual hallucinations and parkinsonian features

63
Q

What drugs can be given in Alzheimers?

A

Acetylcholinesterases eg Donepezil, Rivastigmine

64
Q

What is an epileptic seizure?

A

A convulsion or transient abnormal event from a paroxysmal discharge of cerebral neurones

65
Q

What is the definition of epilepsy?

A

At least 2 unprovoked seizures occurring more than 24hrs apart
One unprovoked seizure and a probability for further seizures similar to general recurrence risk after 2 unprovoked

66
Q

What are causes of an epileptic seizure?

A 
2/3 are idiopathic
CVD eg cerebral infarction
Alcohol withdrawal
Cerebral tumour 
CNS infections 
Metabolic disturbances 
Drugs eg cocaine
67
Q

What are the elements of a seizure?

A

Prodrome = precedes seizure eg change in behaviour
Aura = part of seizure where patient is aware eg strange smell, deja vu or flashing lights
Ictus = the seizure itself
Post ictally = headahce, confusion, sore tongue

68
Q

What are types of primary generalised seizures?

A

Generalised tonic clonic (grand mal) = no aura, loss of conc, tonic phase eg stiff limbs and clonic phase eg rhythmic jerking, may be incontinent and bite tongue and followed by confusion
Typical absence seizure (petit mal) = stare and pale for a few seconds
Myoclonic seizure = sudden isolated jerk of a limb, face or trunk

69
Q

What is the jacksonian march symptom of epilepsy?

A

The seizure starts distally and moves more proximally and is more of motor origin (in frontal lobe seizures)

70
Q

Which anti epileptic is first line for primary generalised tonic clonic seizure?

A

Lamotrigine

71
Q

Which anti epileptic is first line for focal temporal seizure?

A

Carbamazepine

72
Q

When are anti epileptics started?

A

Only if there is a high risk of recurrence

73
Q

What advice should be given to patients with epilepsy?

A

Avoid swimming alone
Leave the door open when taking a bath
Inform the DVLA

74
Q

What is Guillain Barre Syndrome (GBS)?

A

An acute inflammatory demyelination ascending polyneuropathy affecting the peripheral nervous system (schwann cells)

75
Q

What is the aetiology of GBS?

A

75% have a preceding infection of resp/GI tract 1-3 weeks before eg campylobacter jejuni, HIV or EBV

76
Q

How does GBS present?

A

An ascending pattern of progressive symmetrical muscle weakness “toes to nose”
In 20% respiratory and facial muscles are affected putting patients at risk of resp failure

77
Q

How is GBS managed?

A

Monitor FVC hourly and if below 80% admit to ITU
IV immunoglobulins for 5 days and/or plasma exchange
AVOID CORTICOSTEROIDS as make it worse

78
Q

What are common causes of migraines?

A 
C-heese
H-angovers
O-rgasms
C-hocolate
O-ral contraceptive pill
L-ie ins 
A-lcohol
T-umult (loud noise)
E-xercise
79
Q

What are 2 different types of migraines?

A

With aura = progressive neuro deficits that recover completely eg hemianopia, paraesthesia, numbness
Without aura = usually have nausea/vomiting, photophobia or phonophobia (sounds) with headache

80
Q

How are migraines managed?

A

Simple analgesia and anti emetics
Triptans eg sumatriptan
Beta blockers
Tricyclic antideps eg Amitryptiline

81
Q

What is the most common primary headache?

A

Tension headache?

82
Q

What are risk factors of a tension headache?

A

Stress, sleep deprivation, bad posture, hunger, eye strain, anxiety, noise

83
Q

How do cluster headaches present?

A

Rapid onset of severe unilateral headache usually beginning around eye or temple
Pain is unilateral and localised
Ipsilateral cranial autonomic features eg lacrimation, rhinorrhoea (nasal discharge)

84
Q

How are cluster headaches managed?

A 
Acute = inhalation of 100% O2 and triptan (analgesics dont help)
Prophylaxis = CCB eg verapimil, steroids, reduce alcohol and stop smoking
85
Q

How does trigeminal neuralgia present?

A

Severe paroxysms of knife like pain in one or more of the trigeminal nerve divisions
Pain usually shoots from mouth to angle of the jaw
Triggered by stimulation of a specific trigger zone eg by shaving, eating or talking

86
Q

How is trigeminal neuralgia treated?

A

Anticonvulsants eg Carbamazepine

87
Q

What causes trigeminal neuralgia?

A

Compression of the trigeminal nerve by a loop of a vein or artery

88
Q

What is a subarachnoid haemorrhage (SAH)?

A

Spontaneous bleeding into the subarachnoid space (between arachnoid and pia mater)

89
Q

What is the aetiology of SAHs?

A

Rupture of saccular berry aneurysms (80%) usually at branching points in the circle of willis
Congenital arteriovenous malformations eg fistula between arterial and venous systems (10%)
No cause found (15%)

90
Q

How do SAHs present?

A

Sudden onset of a severe occipital “thunder clap” headache eg like being kicked in the head
Vomiting, collapse, seizures and coma
Meningeal irritation

91
Q

How are SAH diagnosed?

A

Gold standard = Head CT showing star shaped lesion and hyperattenuation around circle of willis
Lumbar puncture = xanthocromia

92
Q

How are SAH managed?

A

ABCDE
Give CCB eg Nimodipine to reduce cerebral artery spasm
Prevent re bleeding eg by neurosurgical clipping or endovascular coiling

93
Q

What is a subdural haematoma?

A

An accumulation of blood in the subdural space (between dura and arachnoid mater) due to rupture of a bridging vein

94
Q

What are causes of subdural haematomas?

A

Blunt head trauma with a latent interval after injury eg shaking baby syndrome
Clotting disorders
AV malformations

95
Q

What are risk factors of subdural haematomas?

A

Infants eg due to abuse
Elderly as cerebral atrophy makes brains weaker
Alcoholism

96
Q

How do subdural haematomas present?

A

Fluctuating levels of consciousness
Progressive headache
Raised ICP = vomiting, seizure and raised BP

97
Q

What is shown on a CT head in a subdural?

A

Hyperdense crescent shaped collection of blood over one hemisphere like a banana
Shifting midline structures

98
Q

How are subdural haematomas treated?

A 
Surgical removal
IV Mannitol (diuretic) to reduce ICP
If chronic do burr holes
99
Q

What is an extradural haemorrhage?

A

A collection of blood between the duramater and bone usually caused by a head injury

100
Q

What causes extradural haemorrhages?

A

Usually due to a traumatic head injury which fractures the temporal or parietal bone
The fracture ruptures the underlying middle meningeal artery

101
Q

How do extradural haemorrhages present?

A

Usually have a head injury with brief loss of conc or initial drowsiness followed by a lucid period of recovery and then a rapid decline once the ICP has built up

102
Q

How do extradural haemorrhages appear on CT?

A

A lemon shaped haematoma adjacent to the skull

103
Q

What is Huntingtons Chorea?

A

An autosomal dominant condition (with full penetrance) causing chorea and characterised by a lack of GABA

104
Q

What are clinical manifestations of huntingtons?

A

Often a prodromal phase of mild psychotic and behavioural symptoms eg personality change, clumsiness and apathy
Chorea develops = relentless, progressive jerky involuntary movements
Causes dementia and eventually death

105
Q

What is Lambert Eaton Myasthenic Syndrome?

A

A disorder of neuromuscular transmission caused by impaired presynaptic release of ACh
It causes proximal muscle weakness, autonomic symptoms eg dry mouth, impotence and postural hypotension and eyelid ptosis and mild diplopia

106
Q

What causes lambert eaton myasthenic syndrome?

A

An autoimmune attack against P/Q type voltage gated calcium channels on PREsynaptic neurones

107
Q

What are risk factors of lambert eaton myasthenic syndrome?

A

Cancer = 50% have SCLCs found

108
Q

How is Lambert Eaton Myasthenic Syndrome differentiated from Myasthenia gravis?

A

Detection of ACh receptor antibodies characteristic of myasthenia gravis or malignancy

109
Q

How is Lambert Eaton Myasthenic Syndrome treated?

A

IV 3,4-diaminopyridine which blocks K+ channels improving muscle strength
Immunosuppression by steroids if really severe

110
Q

What is motor neurone disease (MND)?

A

A cluster of major degenerative diseases characterised by destruction of upper and lower motor neurones, cranial nerve nuclei and anterior horn cells in the brain and spinal cord
But no sensory loss, sphincter disturbance or affect on eye movements

111
Q

What are the different types of MND?

A

Amyotrophic lateral sclerosis (AML) 80% = UMN and LMN tends to be focal and asymmetrical in onset
Progressive muscular atrophy (PMA) 10-20% LMN causing weakness and wasting
Progressive bulbar palsy (PBP) 10-20% LMN only lower cranial nerves
Primary lateral sclerosis (PLS) UMN least common

112
Q

What is the management of MND?

A

Antiglutamatergic drugs eg Riluzole a Na channel blocker inhibiting glutamate release and slows progression very slightly
Treat symptoms

113
Q

What is myasthenia gravis?

A

An autoimmune disease against nicotinic acetylcholine receptors in the neuromuscular junction

114
Q

How does myasthenic gravis present?

A

Increasing muscular fatigue on sustained activity
Usually proximal limb muscles, extra ocular muscles and muscles of mastication, speech and facial expression
Ocular palsies, ptosis and diplopia

115
Q

How is myasthenic gravis diagnosed?

A

Elicit fatiguability eg ask to count to 50 and voice will become less audible
Serum anti AChR raised in 90%
Tensilon test positive

116
Q

How is myasthenia gravis treated?

A

Anti cholinesterase eg pyridostigmine to increase ACh in NMJ
Immunosuppression
Thymectomy

117
Q

What is a complication of myasthenic gravis?

A

Weakening of respiratory muscles

118
Q

What is Parkinsons disease?

A

A degenerative movement disorder characterised by a triad of rigidity, bradykinesia and a resting tremor due to reduced DA in the substantia nigra

119
Q

Describe the signs and symptoms present in Parkinsons disease

A 
Resting tremor (4-7Hz) often asymmetrical and most obvious in thumbs eg pill rolling 
Rigidity "cog wheel" 
Bradykinesia = progressive reduction in amplitude of receptive movements, face is expressionless, hypophonia (speech slow and quiet) and micrographia ( writing becomes small 
Postural changes eg stooped, small shuffling steps and reduced asymmetrical arm swing 
Other features = drooling of saliva, depression and constipation
120
Q

How can Parkinsons be managed?

A

If <60 can use DA agonist eg pramipexole or ropinirole to treat motor features and delay starting L-dopa
Gold standard = Levodopa with a peripheral dopa decarboxylase inhibitor eg Madopar preventing peripheral conversion of Ldopa to DA and reducing side effects eg nausea
Over time efficacy is reduced
Monoamine oxidase B inhibitors (MAOIs) eg selegline inhibit MAO enzymes which usually breakdown DA so reduce DA breakdown
COMT inhibitors = similar mechanism as MAOIs

121
Q

What nerve and spinal roots are affected in carpal tunnel syndrome?

A

Median nerve C6-T1

122
Q

Which muscles does the median nerve innervate?

A

LL(2 lumbricals), O(opponens pollicus), A(abductor pollicus brevis), F(flexor pollicus brevis)

123
Q

Which investigations are positive in carpal tunnel syndrome?

A

Phalens test = patient can only maximally flex wrist for 1 min
Tinnels test = tapping on nerve at wrist induces tingling

124
Q

What causes wrist drop?

A

Radial nerve neuropathy (C5-T1)

125
Q

What causes claw hand deformity?

A

Ulnar nerve neuropathy (C7-T1)

126
Q

What causes foot drop?

A

Common peroneal/fibular nerve

127
Q

What signs and symptoms are present in bells palsy?

A 
Unilateral paralysis of the whole side of the face 
Inability to close eye
Hyperacusis (due to noise sensitivity)
Dry mouth 
Loss of taste in anterior 2/3 of tongue
128
Q

How can you differentiate Bells palsy from a stroke?

A

Strokes = forehead sparing because there is bilateral innervation of the forehead so the contralateral lower face is affected only
Bells palsy = no forehead sparing and the whole side of the face is affected unilaterally as it affects the motor innervation after both of the hemispheres have joined

129
Q

How do you manage Bells palsy?

A

Corticosteroids 1st line within 72 hours
Eye protection to prevent corneal injury due to dry eyes
If severe add antiviral

130
Q

What are causes of cauda equina?

A

Herniation of lumbar disc eg at L4/5 or L4/S1
Tumours
Trauma
Infection

131
Q

How does cauda equina present?

A

Flaccid paralysis = LMN signa
Lower limb neuro deficit or lower back pain
Saddle anaesthesia
Bladder/bowel dysfunction

132
Q

What is syncope?

A

A transient LOC due to cerebral hypoperfusion

133
Q

What are causes of syncope?

A

Vasovagal = emotional eg due to fear or pain or orthostatic stress eg prolonged standing
Situational syncope eg due to cough, sneeze or micturition
Orthostatic hypotension
Carotid sinus
Cardiac arryhthmias
Hypoglycaemia

134
Q

What investigations are done for syncope?

A

Orthostatic BP (standing)
ECG
FBC
Tilt testing

135
Q

What is the definition of a TIA?

A

A brief episode of neurological dysfunction due to focal brain, spinal cord or retinal ischaemia without infarction
Duration is no more than 24 hours

136
Q

What risk score is conducted after someone has a TIA?

A 
ABCD2
Age>60
BP>140/90
Clinical features - unilateral weakness (2) or speech disturbance without weakness (1)
Duration of symptoms >60 mins (2) and 10-59 mins (1)
Diabetes 
>6 strongly predicts a stroke 
>4 need assessment within 24 hrs 
All should be seen within 7 days
137
Q

What is Wernickes encephalopathy?

A

A neurological emergency resulting from thiamine (B1) deficiency usually caused by chronic alcohol consumption

138
Q

How does Wernickes encephalopathy present?

A 
Cognitive dysfunction eg loss of memory and confusion
Vision changes eg diplopia
Abnormal gait 
Muscle weakness
Tachycardia 
Asterixis
139
Q

What is Wernicke Korsakoff syndrome?

A

A long term condition that develops when Wernickes encephalopathy is left untreated or not treated soon enough
Causes confusion, memory loss, changes in personality

140
Q

What is strabismus (squint)?

A

A misalignment of the visual axis meaning the eyes aren’t directed at an object at the same time

141
Q

What is radiculopathy?

A

A neurological state in which conduction is limited or blocked along a spinal nerve or its roots

142
Q

What is myelopathy?

A

An injury to the spinal cord due to severe compression of the cord itself

143
Q

What causes sciatica (lumbar radiculopathy)?

A

Compression of the lumbosacral nerve roots L4-S1 forming the sciatic nerve

144
Q

What are the clinical manifestations of sciatica?

A

Unilateral leg pain radiating below the knee to the foot or toes
Low back pain
Numbness or tingling in dermatome
Positive result on a straight leg test

145
Q

What is hydrocephalus?

A

Build up of fluid in the brain/elevated CSF pressure

146
Q

What are clinical features of hydrocephalus?

A

Levodopa unresponsive gait apraxia
Urinary/faecal incontinence
Cognitive impairment

147
Q

What is non epileptic attack disorder?

A

A type of seizure that can look similar to epileptic seizures or fainting but isnt caused by abnormal discharges or blood pressure
They can happen when the brain cant handle thought, memories, emotions or sensations (overwhelming stress)

148
Q

What are clinical manifestations of non epileptic attack disorder?

A

May have tonic clonic seziure like convulsions but movements aren’t rhythmical
Dont lose conc
Last longer than epileptic seizures

149
Q

What is narcolepsy?

A

A chronic condition caused by disruption of the sleep wake cycle and rapid eye movement intrusion in the wake state

150
Q

What are clinical manifestations of narcolepsy?

A 
Excessive daytime sleepiness
Cataplexy (generalised muscle weakness leading to partial or complete collapse)
Sleep paralysis 
Poor memory and conc 
Sleep attacks
151
Q

What are the 3 components of GCS and the maximum scores for each?

A

Eye opening = 4 points
Verbal response = 5 points
Motor response = 6 points

152
Q

What are bulbar palsy?

A

Signs and symptoms linked to impaired function of the lower cranial nerves typically caused by damage to LMNs eg due to tumours or brainstem strokes

3a (3 decks)

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