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COMMON NEUROLOGICAL
DISORDERS AND MANAGEMENT
DR GANESHGOUDA MAJIGOUDRA
CONSULTANT NEUROLOGIST
NANJAPPA HOSPITALS DAVANAGERE
ganeshgoudam4@gmail.com
9380906082
NEUROAXIS BASICS
CLASSIFICATION
ETIOLOGY
V
I
T
A
M
I
N
C
SYMPTOMS
OTHER: Vomiting, altered level of consciousness, memory
problems, LOC, behavioral problems ,abnormal movements, falls etc
COMMON CNS DISORDERS:
Stroke
Seizures
Parkinson's disease
Multiple sclerosis
Head injury
Sleep disorders
Meningitis,Enchephelitis
Tumors
Nutritional deficiency disorders
Developmental disorders
Dementia
Spinal cord infections and inflammation
COMMON PNS DISORDERS
Neuropathy
Myopathy
Myasthenia gravis
NEUROLOGICAL DISEASES - INVESTIGATIONS
• ESR, CBC, CRP,
• Serum biochemistry, Electrolytes, Toxicology screen
• CSF examination and microbiology
• CT scan Brain / MRI Brain or spinal cord
• EEG - Electroencephalography
• Nerve Conduction Studies NCS and EMG – electromyography
• Metabolic disease tests – serum aminoacids and urine organic acids
• Chromosomal studies (Karyotype), Chromosomal miroarray
• Genetic studies – WES - Whole Exome Sequencing (DNA exon analysis)
– WGS - Whole Genome Sequencing (DNA total analysis)
BIOPSY IF NEEDED
DISORDERS OF PERIPHERAL NERVES
NEUROPATHY
 Mononeuropathy
🞑 damage by trauma eg pressure
 Diabetics – nerves sensitive to pressure
🞑 damage to blood supply (vasa nervorum)
 Vasculitic diseases
 Polyneuropathy
🞑 Multiple peripheral nerves
🞑 Distal, symmetrical pattern
🞑 Lower limbs before upper limbs
🞑 Causes -
 Inflammatory
 Metabolic
 toxic
Diabetic neuropathy
 30 – 40% of diabetic patients will develop
significant nerve damage during their lives due to
sub- optimal control
 Small fibre neuropathy
 Autonomic neuropathy
 Motor neuropathy
 Large fibre neuropathy
 Complications
🞑 ulcers
🞑 Infection
Diabetic neuropathy
 Acute painful
neuropathies,
🞑 Constant burning,
parasthesiae, shooting
pains
🞑 Either symmetrical
sensory stocking
distribution
🞑 Contact discomfort (eg.
clothes)
🞑 Insomnia
INVESTIGATIONS AND MANAGEMENT
Nerve compression
🞑 Median nerve compression
In carpal tunnel syndrome occurs in up to
10% patients
 Diagnosis difficult if severe neuropathy involving
hands
 Requires nerve conduction studies
 Surgical decompression
🞑 Ulnar nerve compression
 Usually at elbow (groove of medial epicondyle)
 Pain and paraesthesia along medial aspect of
forearm and numbness in little and ring fingers
🞑 Common peroneal nerve neuropathy
 Nerve runs around head of fibula
 Presents with foot drop and may have wasting of
tibialis anterior (weak foot dorsiflexion, toe
extension and foot eversion)
Guillain-Barre syndrome
 Acute peripheral neuropathy
affecting motor more than
sensory nerves
 Usually follows infection
 Clinical features
🞑 Symptoms over days/weeks
🞑 Bilateral flaccid weakness
🞑 Loss of tendon reflexes
🞑 May affect muscles of respiration
🞑 Burning pains and numbness
INVESTIGATIONS AND MANAGEMENT
NERVE MUSCLE JUNCTION DISORDERS
Myaesthenia gravis
 Autoimmune disorder
 Most patients have antibodies to
acetylcholine receptors at
neuromuscular junction
 Incidence 0.4 in 100000)
 Clinical features
🞑 Fatiguable ptosis
🞑 Diplopia with limitation of eye
movements
🞑 Facial weakness
🞑 Dysphagia
🞑 Dysarthria
🞑 Neck and limb muscle weakness
🞑 Can involve respiratory muscles
INVESTIGATIONS AND MANAGEMENT
MUSCLE DISORDERS
Myopathy
 Weakness of trunk
and proximal limb
muscles
 May be weakness
of neck flexion
and/or extension
and muscles of
facial expression
 Gait waddling
Inflammatory myopathies
 Polymyositis
🞑 May occur in association with
autoimmune connective tissue
disorders
 Dermatomyositis
🞑 Rash affects face and knuckles
🞑 In minority of cases may have
associated malignancy
 Inclusion body myositis
🞑 Selective involvement of finger
flexors and quadriceps
Dermatomyositis
INVESTIGATIONS AND MANAGEMENT
Muscular dystrophy
 Dystrophinopathies
 🞑 Duchenne muscular
dystrophy
 proximal weakness in early
childhood
 Difficulty rising from squatting
position (use hands to ‘climb’
up legs –Gowers’ sign)
 Pseudohypertrophy of calf
 Progressive disability
🞑 Becker muscular dystrophy
 Presents in adolescence or
adult life
 Can have normal lifespan but
progressive disability
🞑 Limb-girdle dystrophies
DISORDERS OF SPINAL CORD
Spinal root disease (radiculopathy)
 Cervical radiculopathy
🞑 Prolapse of intervertebral disc may compress
cervical nerve as exits
🞑 Neck pain, muscle weakness, loss of tendon
reflex, sensory impairment
🞑 Drugs, physiotherapy, may need surgery
 Prolapsed lumbar intervertebral disc
🞑 S1 root
 Low back pain and tenderness
 Pain down leg from buttock to ankle (sciatica)
 Wasting and weakness of gastrocnemius and
soleus)
 S1 sensory loss
 Depressed ankle reflex
🞑 L5 root
 Sciatic pain
 Foot drop (weakness extensor hallucis longus)
 L5 dermatomal sensory impairment
INVESTIGATIONS AND MANAGEMENT
Spinal cord disease
 Inherited
🞑 Hereditary spastic paraplegia
 Congenital
🞑 Arnold-Chiari (develop syringomyelia)
 Trauma
🞑 Disc protrusions, vertebral fracture
 Infection
🞑 Epidural abscess
 Inflammation
🞑 Post-viral transverse myelitis
 Neoplasm
🞑 Vetebral metastases, cord tumour
 Vascular
🞑 Spinal cord infarct, epidural haematoma
 Metabolic
🞑 Subacute combined degeneration of the cord
 Degenerative
🞑 Cord – motor neurone disease
🞑 Spine – spondylosis with cord compression
Spinal dysraphism (spina bifida)
 Failure of closure of neural tube
during development
 Defect of overlying skin
 Abnormal development of bony
structures
 Particularly affects lumbosacral
region
 Myelomeningocoele
🞑 Parts of spinal cord in meningeal
sac
🞑 Paraplegia and incontinence
 Spina bifida occulta
🞑 Mildest form
🞑 Failure of fusion of vertebral
arches
INVESTIGATIONS AND MANAGEMENT
Spinal dysraphism (spina bifida)
 Failure of closure of neural tube
during development
 Defect of overlying skin
 Abnormal development of bony
structures
 Particularly affects lumbosacral
region
 Myelomeningocoele
🞑 Parts of spinal cord in meningeal
sac
🞑 Paraplegia and incontinence
 Spina bifida occulta
🞑 Mildest form
🞑 Failure of fusion of vertebral
arches
INVESTIGATIONS AND MANAGEMENT
DISORDERS OF BRAIN
Multiple sclerosis
 Most common chronic
neurological disorder affecting
young people
 In most typical form is
characterised by lesions
separated in time and space in
central nervous system
 More common in temperate
than tropical climate
 More common in females
(M:F1.5:1)
 Usual age of presentation is
between ages of 20 – 40
 Prevalence of 1 in 1000
Multiple sclerosis
 Pathophysiology
🞑 Affects white matter of brain and
spinal cord
🞑 Inflammatory cells present and
myelin damaged
🞑 Foci of inflammation and
demyelination known as plaques
🞑 Initially inflammation and oedema,
followed by loss of myelin and
then gliosis (scar tissue)
🞑 Leads to reduction in conduction
velocity
🞑 Thought that environmental agent
(eg. virus) triggers condition in
genetically susceptible individual
Multiple sclerosis
 Presentation
🞑 Visual disturbance
 Optic neuritis caused by inflammatory demyelination of one optic
nerve
 Pain around one eye especially on eye movement
 Blurred vision which may progress to monocular blindness over days
or weeks
 Loss of colour vision
🞑 Limb weakness and sensory disturbance
 Lesion in spinal cord or cerebral hemispheres
 May have tingling sensation down back +/or limbs on neck flexion
 Symptoms may be worse after hot bath
Multiple sclerosis
Multiple sclerosis
 Management
🞑 If relapse severe enough to limit function – treat
with steroids
🞑 Symptom control
 Spasticity, fatigue, bladder disturbance, depression,
pain
🞑 Disease modifying therapy
 Interferon beta and glatiramer acetate
Parkinson’s disease
 Degenerative condition affecting extrapyramidal
pathways
(neurotransmitter dopamine)
 Affects dopaminergic neurones in substantia
nigra of midbrain projecting to striatum of
basal ganglia
 Symptoms occur when 60-80% nigrostriate
neurones lost
 Mean age of onset 60 years
 Positive family history
 Clinical triad:
🞑 Akinesia
🞑 Rigidity
🞑 Tremor
Parkinson’s disease
 Gait
🞑 Flexed/stooped
posture
🞑 Difficulty defending
balance
🞑 Difficulty initiating
walking (‘freezing’)
🞑 Steps small and
shuffling
🞑 Festinant
🞑 Normal arm swing lost
🞑 Risk of falls
Parkinson’s disease
 Treatment
🞑 Medical
 Levodopa (often in combination
with DOPAdecarboxylase
inhibitor)
 Dopamine receptor agonists
 Selegiline (monoamine oxidase
inhibitor type B)
 Entacapone (catechol-O-
methyltransferase inhibitor)
 Amantadine
🞑 Surgical
 Stereotactic thalamotomy
(severe tremor)
 Pallidotomy (drug-induced
dyskinesias)
Other movement disorders
 Chorea
🞑 Randomly distributed, irregular timed muscle jerks
 Athetosis
🞑 Inability to sustain body part in one position (eg fingers)
 Tremor
 Dystonia
 Tics
 Drug-induced
 Restless legs syndrome
 Stiff person syndrome
Stroke
 Third most common cause
of death in developed world
(annual incidence 2 per
1000 population)
 Rapidly developing
symptoms or signs
 If resolve within 24 hours –
transient ischaemic attack
Vascular territories
INVESTIGATIONS AND MANAGEMENT
Stroke
 Treatment
🞑 If no haemorrhage start aspirin
🞑 Clopidogrel can be used in patients intolerant of aspirin
🞑 Thrombolysis
 iv tissue plasminogen activator (alteplase/tenecteplase)
 Within 4.5 hours of stroke onset
 Prevention
🞑 Modify risk factors
 Smoking
 Diet (inc lower cholesterol)
 Blood pressure
 Diabetic control
Stroke
 Complications
🞑 Pneumonia
🞑 Deep venous thrombosis and pulmonary embolism
🞑 Myocardial infarction
🞑 10% of patients with cerebral infarction die in first 30 days post-
stroke
🞑 50% remain dependent
🞑 Long-term disability
 Pressure sores, seizures, falls, spasticity, depression
Subarachnoid haemorrhage
 Causes
🞑 Rupture of aneurysm
🞑 Arteriovenous malformation
🞑 Trauma
🞑 Blood vessels weakened by infection
(v rare)
 Features
🞑 Sudden severe headache with
photophobia, vomiting, neck
stiffness
 Management
🞑 30-40% die within few days of onset
🞑 Signif risk of rebleeding in 6 weeks
after onset
🞑 Nimodipine
🞑 Aneurysm clipped or coiled
Intracerebral haemorrhage
 10% of all strokes
 Large haematomas have poor prognosis (>50%
mortality) – risk of hydrocephalus and coning
 Causes
🞑 Hypertension
🞑 Bleeding into tumours
🞑 Trauma
🞑 Blood disorders
🞑 Blood vessel disorders
INVESTIGATIONS AND MANAGEMENT
Epilepsy
 1% of population suffer from
epilepsy
 Definition
🞑 ‘ paroxysmal disorder in which
cerebral cortical neuronal
discharges result in intermittent,
stereotyped attacks of altered
consciousness, motor or
sensory function, behaviour or
emotion’
 Classification
🞑 Partial (simple or complex)
🞑 Generalised (absence,
myoclonic, tonic-clonic, tonic,
atonic)
Convulsions
Partial seizures/focal seizures
 Simple partial seizure/Focal aware
🞑 Arise in one cortical area (most commonly temporal lobes)
🞑 Usually brief
🞑 Discharge remains localised (eg focal motor, sensory or psychic
symptoms)
🞑 No loss of awareness
 Complex partial seizure/focal impaired aware
🞑 Impairment of awareness during attack
🞑 Frequently altered or ‘autonomic’ behaviour
🞑 Reactive automatisms – may be able to do simple task
 Partial onset with secondary generalisation/ focal to BL
🞑 Epileptic discharge spreads to both cerebral hemispheres
Generalised seizures
 Absence
 Myoclonic
 Clonic
 Tonic
 Tonic-clonic
 Atonic
Tonic-clonic seizures
 May have prodrome or no warning
 Tonic phase – rigidity
 Often cyanosed
 Clonic phase – jerking (about 2 mins)
 May be incontinent or bite cheek/tongue
 Post-ictal confusion and tiredness
INVESTIGATIONS AND MANAGEMENT
Conditions that mimic epilepsy
 Syncope
🞑 Lasts <30 secs, pale, little/no confusion after event
 Cardiac
🞑 arrhythmia, outflow obstruction
 Transient ischaemic attacks
🞑 Usually last longer, rarely LOC
 Metabolic disturbance
 Non-epileptic attacks
Headache and facial pain
 Headache
🞑 Primary (uncertain
cause)
 Migraine
 Cluster headache
 Tension-type
🞑 Secondary (known
cause)
 Raised ICP
 Idiopathic
intracranial
hypertension
 Meningeal irritation
 Giant cell arteritis
 Metabolic
disturbances
 Facial pain
🞑 Trigeminal neualgia
🞑 Post-herpetic
neuralgia
Migraine
 Unilateral headache
 Associated with nausea, vomiting, visual disturbance
 Typical onset teens and twenties
 Aura may be phase of vasoconstriction
 Then vasodilatation of extracerebral vessels may cause
headache
 Treatment
🞑 simple analgesia initially
🞑 triptan (5HT1 R agonist)
🞑 Prophylactic agents
 Propranolol
 Flunarazine
INVESTIGATIONS AND MANAGEMENT
Other headaches
 Cluster headache
🞑 Unilateral headache
🞑 Severe attacks pain around one eye
🞑 Lasts 20 – 120 mins
🞑 Usually recurs several times a day
🞑 Pattern continues for days, weeks or months
🞑 Then symptom-free for weeks-months
🞑 Treatment
 Steroids initially, then verapamil
 Tension-type headache/ chronic daily
headache
🞑 May be due to neck muscle contraction
🞑 Amitriptyline may help
Facial pain
 Trigeminal neuralgia
🞑 Compression of trigeminal sensory root
🞑 Unilateral facial pain with trigger areas
🞑 Treat with carbamazepine initially
🞑 May require surgery
 Post-herpetic neuralgia
🞑 Post-shingles of a branch of trigeminal nerve
🞑 Persistent facial pain after rash healed
🞑 May respond to amitriptyline, carbamazepine
INVESTIGATIONS AND MANAGEMENT
Neurological infections
 Bacterial
🞑 Meningitis
 Neisseria meningitidis, Streptococcus
🞑 Brain
abscess
 May complicate otitis media
 Raised intracranial pressure, focal signs, seizures
🞑 Parameningeal infections
 Pus in epidural space
🞑 Tuberculosis
🞑 Syphilis
🞑 Lyme disease
🞑 Leprosy
Neurological infections
 Viral infections
🞑 Viral meningitis
 Mumps, enterovirus
🞑 Viral encephalitis
 Commonest cause Herpes simplex
 Headache, fever, reduced LOC, may have seizures
🞑 Herpes zoster
 Dormant in dorsal root ganglion after chickenpox
 May reactivate as shingles
 Pain and itching of single or adjacent dermatomes, following by
vesicular rash
🞑 Retroviral infections
 Meningitic illness may occur at seroconversion
 Slowly progressive dementia
 Risks of immunocompromise (infection, tumour)
INVESTIGATIONS AND MANAGEMENT
Head injury
 Damage at impact
🞑 Contusion and
laceration
🞑 Diffuse axonal injury
 Secondary
complications
🞑 Haematoma
🞑 Cerebral oedema
🞑 Cerebral ischaemia
🞑 Coning
🞑 Infection
🞑 Post-traumatic
epilepsy
INVESTIGATIONS AND MANAGEMENT
Brain tumour
 Intracranial neoplasms:
🞑 Benign
 Usually extra-axial (eg. Meninges, cranial nerves)
 Compress brain
🞑 Malignant
 Usually intra-axial (ie. brain parenchyma)
 Primary (>50% adult intracranial neoplasms)
 gliomas
 Secondary (15-20% adult intracranial neoplasms)
 metastases
Glioma
Brain tumour - management
 Surgery
🞑 Benign tumours
 Complete excision may be possible -cure
🞑 Malignant
 Histology
 Symptomatic
 Radiotherapy
🞑 Gliomas – direct towards tumour
🞑 Metastases – whole-brain radiation
 Drug treatment
🞑 Anti-convulsants
🞑 Dexamethasone
🞑 Chemotherapy
Congenital disorders
 Cerebral palsy
 Spinal dysraphism
 Infantile hydrocephalus
 Cerebral structural disorders
 Intrauterine infection
Cerebral palsy
 Pre- or peri-natal insult
🞑 Fetal hypoxia or infection
🞑 Prematurity
🞑 Traumatic delivery
 Clinical features:
🞑 Spastic diplegia
 May have shortening and deformity of
legs
🞑 Spastic hemiplegia
 Associated with hemisensory deficits,
learning difficulties and
epilepsy
🞑 Athetoid cerebral palsy
 Movement disorder develops in early
childhood. Usually normal cognitive
function
Developmental delay / Intellectual handicap
• Cerebral Palsy
• Delayed development
• Intellectual handicap
INVESTIGATIONS AND MANAGEMENT
Neurogenetics
 Huntington’s disease
 Wilson’s disease
 Friedreich’s ataxia
 Hereditary spastic paraplegia
 Leber’s hereditary optic atrophy
 Hereditary spinal muscular
atrophies
 Hereditary motor and sensory
neuropathy (HMSN)
 Muscular dystrophies
INVESTIGATIONS AND MANAGEMENT
NEWER DRUGS APPROVED
OMAVELOXOLONE -- FA
NUSINERSIN-- SMA
GOLODIRSEN &VILTOLARSEN --DMD
Dementia
 Inherited
🞑 FamilialAlzheimer’s disease,
Huntington’s disease
 Trauma
 Infection
🞑 Syphilis,AIDS-related,
 Inflammation
🞑 Multiple sclerosis
 Neoplasm
🞑 Frontal tumours
 Vascular
🞑 Multi-infarct dementia
 Metabolic
🞑 hypothyroidism
 Drugs/toxins
🞑 Barbiturates, alcohol
 Degenerative
🞑 Alzheimer’s disease, Prion disease
INVESTIGATIONS AND MANAGEMENT
Neurorehabilitation
 Aim ‘to restore patients to maximum capability and
independence within limits set by their disability and
their needs’
 Multidisciplinary teams
🞑 Physiotherapy
🞑 Occupational therapy
🞑 Speech therapy
🞑 Neuropsychology
🞑 Social work
THANK YOU
Videos…………
ganeshgoudam4@gmail.com
9380906082

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Common Neurological Disorders for undergraduates( MBBS, NURSING,PHRMA STUDENTS) DR Ganesh.pptx

  • 1. COMMON NEUROLOGICAL DISORDERS AND MANAGEMENT DR GANESHGOUDA MAJIGOUDRA CONSULTANT NEUROLOGIST NANJAPPA HOSPITALS DAVANAGERE ganeshgoudam4@gmail.com 9380906082
  • 5. SYMPTOMS OTHER: Vomiting, altered level of consciousness, memory problems, LOC, behavioral problems ,abnormal movements, falls etc
  • 6. COMMON CNS DISORDERS: Stroke Seizures Parkinson's disease Multiple sclerosis Head injury Sleep disorders Meningitis,Enchephelitis Tumors Nutritional deficiency disorders Developmental disorders Dementia Spinal cord infections and inflammation
  • 8. NEUROLOGICAL DISEASES - INVESTIGATIONS • ESR, CBC, CRP, • Serum biochemistry, Electrolytes, Toxicology screen • CSF examination and microbiology • CT scan Brain / MRI Brain or spinal cord • EEG - Electroencephalography • Nerve Conduction Studies NCS and EMG – electromyography • Metabolic disease tests – serum aminoacids and urine organic acids • Chromosomal studies (Karyotype), Chromosomal miroarray • Genetic studies – WES - Whole Exome Sequencing (DNA exon analysis) – WGS - Whole Genome Sequencing (DNA total analysis) BIOPSY IF NEEDED
  • 10. NEUROPATHY  Mononeuropathy 🞑 damage by trauma eg pressure  Diabetics – nerves sensitive to pressure 🞑 damage to blood supply (vasa nervorum)  Vasculitic diseases  Polyneuropathy 🞑 Multiple peripheral nerves 🞑 Distal, symmetrical pattern 🞑 Lower limbs before upper limbs 🞑 Causes -  Inflammatory  Metabolic  toxic
  • 11. Diabetic neuropathy  30 – 40% of diabetic patients will develop significant nerve damage during their lives due to sub- optimal control  Small fibre neuropathy  Autonomic neuropathy  Motor neuropathy  Large fibre neuropathy  Complications 🞑 ulcers 🞑 Infection
  • 12. Diabetic neuropathy  Acute painful neuropathies, 🞑 Constant burning, parasthesiae, shooting pains 🞑 Either symmetrical sensory stocking distribution 🞑 Contact discomfort (eg. clothes) 🞑 Insomnia INVESTIGATIONS AND MANAGEMENT
  • 13. Nerve compression 🞑 Median nerve compression In carpal tunnel syndrome occurs in up to 10% patients  Diagnosis difficult if severe neuropathy involving hands  Requires nerve conduction studies  Surgical decompression 🞑 Ulnar nerve compression  Usually at elbow (groove of medial epicondyle)  Pain and paraesthesia along medial aspect of forearm and numbness in little and ring fingers 🞑 Common peroneal nerve neuropathy  Nerve runs around head of fibula  Presents with foot drop and may have wasting of tibialis anterior (weak foot dorsiflexion, toe extension and foot eversion)
  • 14. Guillain-Barre syndrome  Acute peripheral neuropathy affecting motor more than sensory nerves  Usually follows infection  Clinical features 🞑 Symptoms over days/weeks 🞑 Bilateral flaccid weakness 🞑 Loss of tendon reflexes 🞑 May affect muscles of respiration 🞑 Burning pains and numbness INVESTIGATIONS AND MANAGEMENT
  • 16. Myaesthenia gravis  Autoimmune disorder  Most patients have antibodies to acetylcholine receptors at neuromuscular junction  Incidence 0.4 in 100000)  Clinical features 🞑 Fatiguable ptosis 🞑 Diplopia with limitation of eye movements 🞑 Facial weakness 🞑 Dysphagia 🞑 Dysarthria 🞑 Neck and limb muscle weakness 🞑 Can involve respiratory muscles INVESTIGATIONS AND MANAGEMENT
  • 18. Myopathy  Weakness of trunk and proximal limb muscles  May be weakness of neck flexion and/or extension and muscles of facial expression  Gait waddling
  • 19. Inflammatory myopathies  Polymyositis 🞑 May occur in association with autoimmune connective tissue disorders  Dermatomyositis 🞑 Rash affects face and knuckles 🞑 In minority of cases may have associated malignancy  Inclusion body myositis 🞑 Selective involvement of finger flexors and quadriceps
  • 21. Muscular dystrophy  Dystrophinopathies  🞑 Duchenne muscular dystrophy  proximal weakness in early childhood  Difficulty rising from squatting position (use hands to ‘climb’ up legs –Gowers’ sign)  Pseudohypertrophy of calf  Progressive disability 🞑 Becker muscular dystrophy  Presents in adolescence or adult life  Can have normal lifespan but progressive disability 🞑 Limb-girdle dystrophies
  • 22.
  • 23.
  • 25. Spinal root disease (radiculopathy)  Cervical radiculopathy 🞑 Prolapse of intervertebral disc may compress cervical nerve as exits 🞑 Neck pain, muscle weakness, loss of tendon reflex, sensory impairment 🞑 Drugs, physiotherapy, may need surgery  Prolapsed lumbar intervertebral disc 🞑 S1 root  Low back pain and tenderness  Pain down leg from buttock to ankle (sciatica)  Wasting and weakness of gastrocnemius and soleus)  S1 sensory loss  Depressed ankle reflex 🞑 L5 root  Sciatic pain  Foot drop (weakness extensor hallucis longus)  L5 dermatomal sensory impairment INVESTIGATIONS AND MANAGEMENT
  • 26. Spinal cord disease  Inherited 🞑 Hereditary spastic paraplegia  Congenital 🞑 Arnold-Chiari (develop syringomyelia)  Trauma 🞑 Disc protrusions, vertebral fracture  Infection 🞑 Epidural abscess  Inflammation 🞑 Post-viral transverse myelitis  Neoplasm 🞑 Vetebral metastases, cord tumour  Vascular 🞑 Spinal cord infarct, epidural haematoma  Metabolic 🞑 Subacute combined degeneration of the cord  Degenerative 🞑 Cord – motor neurone disease 🞑 Spine – spondylosis with cord compression
  • 27. Spinal dysraphism (spina bifida)  Failure of closure of neural tube during development  Defect of overlying skin  Abnormal development of bony structures  Particularly affects lumbosacral region  Myelomeningocoele 🞑 Parts of spinal cord in meningeal sac 🞑 Paraplegia and incontinence  Spina bifida occulta 🞑 Mildest form 🞑 Failure of fusion of vertebral arches INVESTIGATIONS AND MANAGEMENT
  • 28. Spinal dysraphism (spina bifida)  Failure of closure of neural tube during development  Defect of overlying skin  Abnormal development of bony structures  Particularly affects lumbosacral region  Myelomeningocoele 🞑 Parts of spinal cord in meningeal sac 🞑 Paraplegia and incontinence  Spina bifida occulta 🞑 Mildest form 🞑 Failure of fusion of vertebral arches INVESTIGATIONS AND MANAGEMENT
  • 30. Multiple sclerosis  Most common chronic neurological disorder affecting young people  In most typical form is characterised by lesions separated in time and space in central nervous system  More common in temperate than tropical climate  More common in females (M:F1.5:1)  Usual age of presentation is between ages of 20 – 40  Prevalence of 1 in 1000
  • 31. Multiple sclerosis  Pathophysiology 🞑 Affects white matter of brain and spinal cord 🞑 Inflammatory cells present and myelin damaged 🞑 Foci of inflammation and demyelination known as plaques 🞑 Initially inflammation and oedema, followed by loss of myelin and then gliosis (scar tissue) 🞑 Leads to reduction in conduction velocity 🞑 Thought that environmental agent (eg. virus) triggers condition in genetically susceptible individual
  • 32. Multiple sclerosis  Presentation 🞑 Visual disturbance  Optic neuritis caused by inflammatory demyelination of one optic nerve  Pain around one eye especially on eye movement  Blurred vision which may progress to monocular blindness over days or weeks  Loss of colour vision 🞑 Limb weakness and sensory disturbance  Lesion in spinal cord or cerebral hemispheres  May have tingling sensation down back +/or limbs on neck flexion  Symptoms may be worse after hot bath
  • 34. Multiple sclerosis  Management 🞑 If relapse severe enough to limit function – treat with steroids 🞑 Symptom control  Spasticity, fatigue, bladder disturbance, depression, pain 🞑 Disease modifying therapy  Interferon beta and glatiramer acetate
  • 35. Parkinson’s disease  Degenerative condition affecting extrapyramidal pathways (neurotransmitter dopamine)  Affects dopaminergic neurones in substantia nigra of midbrain projecting to striatum of basal ganglia  Symptoms occur when 60-80% nigrostriate neurones lost  Mean age of onset 60 years  Positive family history  Clinical triad: 🞑 Akinesia 🞑 Rigidity 🞑 Tremor
  • 36. Parkinson’s disease  Gait 🞑 Flexed/stooped posture 🞑 Difficulty defending balance 🞑 Difficulty initiating walking (‘freezing’) 🞑 Steps small and shuffling 🞑 Festinant 🞑 Normal arm swing lost 🞑 Risk of falls
  • 37. Parkinson’s disease  Treatment 🞑 Medical  Levodopa (often in combination with DOPAdecarboxylase inhibitor)  Dopamine receptor agonists  Selegiline (monoamine oxidase inhibitor type B)  Entacapone (catechol-O- methyltransferase inhibitor)  Amantadine 🞑 Surgical  Stereotactic thalamotomy (severe tremor)  Pallidotomy (drug-induced dyskinesias)
  • 38. Other movement disorders  Chorea 🞑 Randomly distributed, irregular timed muscle jerks  Athetosis 🞑 Inability to sustain body part in one position (eg fingers)  Tremor  Dystonia  Tics  Drug-induced  Restless legs syndrome  Stiff person syndrome
  • 39. Stroke  Third most common cause of death in developed world (annual incidence 2 per 1000 population)  Rapidly developing symptoms or signs  If resolve within 24 hours – transient ischaemic attack
  • 42. Stroke  Treatment 🞑 If no haemorrhage start aspirin 🞑 Clopidogrel can be used in patients intolerant of aspirin 🞑 Thrombolysis  iv tissue plasminogen activator (alteplase/tenecteplase)  Within 4.5 hours of stroke onset  Prevention 🞑 Modify risk factors  Smoking  Diet (inc lower cholesterol)  Blood pressure  Diabetic control
  • 43. Stroke  Complications 🞑 Pneumonia 🞑 Deep venous thrombosis and pulmonary embolism 🞑 Myocardial infarction 🞑 10% of patients with cerebral infarction die in first 30 days post- stroke 🞑 50% remain dependent 🞑 Long-term disability  Pressure sores, seizures, falls, spasticity, depression
  • 44. Subarachnoid haemorrhage  Causes 🞑 Rupture of aneurysm 🞑 Arteriovenous malformation 🞑 Trauma 🞑 Blood vessels weakened by infection (v rare)  Features 🞑 Sudden severe headache with photophobia, vomiting, neck stiffness  Management 🞑 30-40% die within few days of onset 🞑 Signif risk of rebleeding in 6 weeks after onset 🞑 Nimodipine 🞑 Aneurysm clipped or coiled
  • 45. Intracerebral haemorrhage  10% of all strokes  Large haematomas have poor prognosis (>50% mortality) – risk of hydrocephalus and coning  Causes 🞑 Hypertension 🞑 Bleeding into tumours 🞑 Trauma 🞑 Blood disorders 🞑 Blood vessel disorders INVESTIGATIONS AND MANAGEMENT
  • 46. Epilepsy  1% of population suffer from epilepsy  Definition 🞑 ‘ paroxysmal disorder in which cerebral cortical neuronal discharges result in intermittent, stereotyped attacks of altered consciousness, motor or sensory function, behaviour or emotion’  Classification 🞑 Partial (simple or complex) 🞑 Generalised (absence, myoclonic, tonic-clonic, tonic, atonic)
  • 48. Partial seizures/focal seizures  Simple partial seizure/Focal aware 🞑 Arise in one cortical area (most commonly temporal lobes) 🞑 Usually brief 🞑 Discharge remains localised (eg focal motor, sensory or psychic symptoms) 🞑 No loss of awareness  Complex partial seizure/focal impaired aware 🞑 Impairment of awareness during attack 🞑 Frequently altered or ‘autonomic’ behaviour 🞑 Reactive automatisms – may be able to do simple task  Partial onset with secondary generalisation/ focal to BL 🞑 Epileptic discharge spreads to both cerebral hemispheres
  • 49. Generalised seizures  Absence  Myoclonic  Clonic  Tonic  Tonic-clonic  Atonic
  • 50. Tonic-clonic seizures  May have prodrome or no warning  Tonic phase – rigidity  Often cyanosed  Clonic phase – jerking (about 2 mins)  May be incontinent or bite cheek/tongue  Post-ictal confusion and tiredness INVESTIGATIONS AND MANAGEMENT
  • 51. Conditions that mimic epilepsy  Syncope 🞑 Lasts <30 secs, pale, little/no confusion after event  Cardiac 🞑 arrhythmia, outflow obstruction  Transient ischaemic attacks 🞑 Usually last longer, rarely LOC  Metabolic disturbance  Non-epileptic attacks
  • 52. Headache and facial pain  Headache 🞑 Primary (uncertain cause)  Migraine  Cluster headache  Tension-type 🞑 Secondary (known cause)  Raised ICP  Idiopathic intracranial hypertension  Meningeal irritation  Giant cell arteritis  Metabolic disturbances  Facial pain 🞑 Trigeminal neualgia 🞑 Post-herpetic neuralgia
  • 53. Migraine  Unilateral headache  Associated with nausea, vomiting, visual disturbance  Typical onset teens and twenties  Aura may be phase of vasoconstriction  Then vasodilatation of extracerebral vessels may cause headache  Treatment 🞑 simple analgesia initially 🞑 triptan (5HT1 R agonist) 🞑 Prophylactic agents  Propranolol  Flunarazine INVESTIGATIONS AND MANAGEMENT
  • 54. Other headaches  Cluster headache 🞑 Unilateral headache 🞑 Severe attacks pain around one eye 🞑 Lasts 20 – 120 mins 🞑 Usually recurs several times a day 🞑 Pattern continues for days, weeks or months 🞑 Then symptom-free for weeks-months 🞑 Treatment  Steroids initially, then verapamil  Tension-type headache/ chronic daily headache 🞑 May be due to neck muscle contraction 🞑 Amitriptyline may help
  • 55. Facial pain  Trigeminal neuralgia 🞑 Compression of trigeminal sensory root 🞑 Unilateral facial pain with trigger areas 🞑 Treat with carbamazepine initially 🞑 May require surgery  Post-herpetic neuralgia 🞑 Post-shingles of a branch of trigeminal nerve 🞑 Persistent facial pain after rash healed 🞑 May respond to amitriptyline, carbamazepine INVESTIGATIONS AND MANAGEMENT
  • 56. Neurological infections  Bacterial 🞑 Meningitis  Neisseria meningitidis, Streptococcus 🞑 Brain abscess  May complicate otitis media  Raised intracranial pressure, focal signs, seizures 🞑 Parameningeal infections  Pus in epidural space 🞑 Tuberculosis 🞑 Syphilis 🞑 Lyme disease 🞑 Leprosy
  • 57. Neurological infections  Viral infections 🞑 Viral meningitis  Mumps, enterovirus 🞑 Viral encephalitis  Commonest cause Herpes simplex  Headache, fever, reduced LOC, may have seizures 🞑 Herpes zoster  Dormant in dorsal root ganglion after chickenpox  May reactivate as shingles  Pain and itching of single or adjacent dermatomes, following by vesicular rash 🞑 Retroviral infections  Meningitic illness may occur at seroconversion  Slowly progressive dementia  Risks of immunocompromise (infection, tumour) INVESTIGATIONS AND MANAGEMENT
  • 58. Head injury  Damage at impact 🞑 Contusion and laceration 🞑 Diffuse axonal injury  Secondary complications 🞑 Haematoma 🞑 Cerebral oedema 🞑 Cerebral ischaemia 🞑 Coning 🞑 Infection 🞑 Post-traumatic epilepsy INVESTIGATIONS AND MANAGEMENT
  • 59. Brain tumour  Intracranial neoplasms: 🞑 Benign  Usually extra-axial (eg. Meninges, cranial nerves)  Compress brain 🞑 Malignant  Usually intra-axial (ie. brain parenchyma)  Primary (>50% adult intracranial neoplasms)  gliomas  Secondary (15-20% adult intracranial neoplasms)  metastases
  • 61. Brain tumour - management  Surgery 🞑 Benign tumours  Complete excision may be possible -cure 🞑 Malignant  Histology  Symptomatic  Radiotherapy 🞑 Gliomas – direct towards tumour 🞑 Metastases – whole-brain radiation  Drug treatment 🞑 Anti-convulsants 🞑 Dexamethasone 🞑 Chemotherapy
  • 62. Congenital disorders  Cerebral palsy  Spinal dysraphism  Infantile hydrocephalus  Cerebral structural disorders  Intrauterine infection
  • 63. Cerebral palsy  Pre- or peri-natal insult 🞑 Fetal hypoxia or infection 🞑 Prematurity 🞑 Traumatic delivery  Clinical features: 🞑 Spastic diplegia  May have shortening and deformity of legs 🞑 Spastic hemiplegia  Associated with hemisensory deficits, learning difficulties and epilepsy 🞑 Athetoid cerebral palsy  Movement disorder develops in early childhood. Usually normal cognitive function
  • 64. Developmental delay / Intellectual handicap • Cerebral Palsy • Delayed development • Intellectual handicap INVESTIGATIONS AND MANAGEMENT
  • 65. Neurogenetics  Huntington’s disease  Wilson’s disease  Friedreich’s ataxia  Hereditary spastic paraplegia  Leber’s hereditary optic atrophy  Hereditary spinal muscular atrophies  Hereditary motor and sensory neuropathy (HMSN)  Muscular dystrophies INVESTIGATIONS AND MANAGEMENT
  • 66. NEWER DRUGS APPROVED OMAVELOXOLONE -- FA NUSINERSIN-- SMA GOLODIRSEN &VILTOLARSEN --DMD
  • 67. Dementia  Inherited 🞑 FamilialAlzheimer’s disease, Huntington’s disease  Trauma  Infection 🞑 Syphilis,AIDS-related,  Inflammation 🞑 Multiple sclerosis  Neoplasm 🞑 Frontal tumours  Vascular 🞑 Multi-infarct dementia  Metabolic 🞑 hypothyroidism  Drugs/toxins 🞑 Barbiturates, alcohol  Degenerative 🞑 Alzheimer’s disease, Prion disease INVESTIGATIONS AND MANAGEMENT
  • 68. Neurorehabilitation  Aim ‘to restore patients to maximum capability and independence within limits set by their disability and their needs’  Multidisciplinary teams 🞑 Physiotherapy 🞑 Occupational therapy 🞑 Speech therapy 🞑 Neuropsychology 🞑 Social work