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Neurology Notes

Medicine Notes > Paediatrics Notes

This is an extract of our Neurology document, which we sell as part of our Paediatrics Notes collection written by the top tier of University Of Nottingham students.

The following is a more accessble plain text extract of the PDF sample above, taken from our Paediatrics Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:

Neurology Cerebral Palsy

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Abnormality of movement or posture attributed to non progressive disturbances that occurred in the developing fetal or infant brain

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Presents in early life (<2 years)

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Accompanied by disturbances of cognition, communication, perception, sensation, behaviour and seziure disorder and secondary MSK problems

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Affects 2 in 1000 live births

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Althought the underlying cause is static, the resulting motor disorder may evolve, giving the impression of deterioration

Causes

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80% are antenatal in origin

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10% due to hypoxicischaemic injury during delivery

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10% are postnatal after the age of 2 it is more appropriate to use acuired brain injury

o

Meningitis/encephalitis/encephalopathy

o

Trauma

o

Symptomatic hypoglycaemia

o

Hydrocephalus

o

Hyperbilirubinaemia

Clinical Presentation (see pg 55 of Illustrated)

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Early features

o

Abnormal limb/trunk posture and toneo

Feeding difficult*

Delayed motor milestones

Oromotor incoordination, slow feeding, gagging and vomiting

o

Abnormal gait

o

Asymmetric hand function before 12 months

Functional ability described using the Gross Motor Function Classification System

o

I; walks without limtations

o

II; walks with limitations

o

III; uses handheld mobility device

o

IV; self mobility with limitations; powered mobility

o

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V; manual wheelchair

Diagnosis made by clinical examination 3 clinical subtypes

o

Spastic (90%)

o

Dyskinetic

o

Ataxic

Spastic

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UMN damage (pyramidal or corticospinal tract)

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Clinically

o

o

Increased limb toneVelocity dependent stretch muscle faster = greater resistanceMay suddenly yield under pressure catch phenomenon

Brisk deep tendon reflexes*

Extensor plantars

3 main types

o

o

o

Hemiplegia412 months of ageFisting of affected handFlexed arm and pronated forearmHip flexion and internal rotationToeheel walk on affected side

QuadripleguaOpisothonus (extensor posturing)Severe hence associated features

DiplegiaAll 4 limbs but legs are worseAssociated with preterm birth and periventricular damage

Dyskinetic

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Damage in the basal ganglia

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Previous common cause was hyperbilirubinaemia (kernicerus)

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Involuntary, uncontrolled, stereotyped movements

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Most evident with active movement or stress

*

*

May be described as

o

Chorea irregular, sudden, brief, non repetative

o

Athetosis slow writhing

o

Dystonia simultaneous agonist and antagonist contraction

Present with

o

Floppiness

o

Poor trunk control

o

Delayed devlopment

Ataxic (hypotonic)

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Trunk and limb hypotonia

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Poor balance

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Delayed development

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Incoordinate movements, intention tremor and ataxic gait

Seizures

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Sudden disturbance of neurological function caused by adnormal or excessive discharge

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May be EPILEPTICAL

*

o

Idiopathic (7080%)

o

SecondaryCerebral dysgenesis/malformationCerebral vascular occlusionCerebral damage

o

Tumour

o

Neurodegenerative disorders

o

Neurocutaneous syndromes

NON EPILEPTIC

o

Febrile

o

Syncopal (anoxic)

o

Brainstem (hydrocephalic, coning)

o

Emotional (psychogenic, pseudo)

o

MetabolicHypoglycaemia. Etc.

o

Head trauma

o

Meningitis / encephalitis

o

Poisons / toxins

Febrile Seizures

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Seizure accompanied by fever in the ABSENCE of intracranial infection due to bacterial meningitis or viral encephalitis

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Often associated with URTI

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3% of children aged between 6 months and 6 years

o

Unusual after >4 years

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Family history often present (?genetic)

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Seizures are typically brief

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Generalised tonicclonic seizures

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30% recur

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Does not cause brain damage

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Investigations lumbar puncture - low threshold

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If there is history of a prolonged seizure (>10 minutes) rescue therapy with diazepam PR of midazolam (buccal)

Paroxysmal Disorders

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"Funny turns"

Breath Holding Attacks

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In toddlers when upset

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Child may lose consciousness but rapidly recover

Reflex Anoxic Seizure

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Infants and toddlers

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Family history

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Triggers

*

o

Pain (esp. from minor head trauma)

o

Cold food

o

Fright

o

Fever

After the event the child becomes pale and falls to the floor due to cardiac asystole from vagal inhibition

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Hypoxia may induce a generalised tonic clonic seizure

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Brief and child recovers

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NB; ocular compression under controlled conditions may lead to asystole and paroxysmal slow wave discharge on ECG

Others

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Benign Paroxysmal Vertigo

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Due to viral labyrinthitis

*

Associated with nystagmus, unsteadiness and loss of balnce

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Cardiac Arrhythmia

o

Prolonged QT interval may rarely cause collapse or cardiac syncope

*

Syncope

*

Migraine

*

Selfgratification

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Sleep disorders sleep myoclonus, parasomnias

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Daydreaming

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Pseudoseizures

Epilepsy

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Largely classified as generalised or focal seizures

Generalised

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ALWAYS a loss of consciousness

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No warning

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Symmetricaly

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Absence

*

*

o

Transient loss of consciousness

o

Abrupt onset and termination

o

No motor phenomena

Myoclonic

o

Brief, repetitive, jerking movement of the limbs, neck or trunk

o

Physiological stage II sleep sleep myoclonus

Tonic

o

*

Generalised increase in tone

Tonicclonic

o

Rhythmical contraction following the tonic phase

o

Rigid tonic phase children do not breath may become cyanosed

o

Clonic phase breathing is irregular, cyanosis persists and saliva may accumulate, biting of toungue and incontinence

*

o

Lasts seconds to minutes

o

Followed by unconsciousness or deep sleep for up to several hours

Atonic

o

Loss of muscle tone

Focal

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May be preceded by an aura

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May or may not be associated with a change in consciousness or more generalised tonicclonic seizure

*

Frontal motor

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Temporal auditory / sensory (smell or taste). Automatisms (lip smacking. Etc.) occur after spread to the frontal lobe. Dejavu associated

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Occipital visual

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Parietal contralateral altered sensation (dysaesthsia)

Diagnosis

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Diagnosis primarily based upon history

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Clinical examination should involve checking for skin markings suggesting neurocutaneous syndrome or neurological abnormalities

*

EEG

*

Imaging

o

Structural not required unless there are neurological signs between seizures or seizures are focalMRI FLAIR (fluid attenuated inversion recovery) sequences better detct mesial temporal sclerosis

o

FunctionalPET and SPECTBoth can detect areas of hypometabolism in epileptogenic lesionsSPECT can be used to capture seizures and areas of hypermetabolism

Management

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Common not to start treatment after only one episode

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Anti Epileptic Drugs (AED) Therapy

o

Typically discontinued after 2 years symptoms free

o

Prolonged seizures may require rescue therapyDiazepam PRMidazolam (buccal)

Seizure Type Generalised

*

Tonic Clonic

*

Absence

*

Myoclonic

Focal

First Line

Second Line

Valporate, carbamazepine

Lamotrigine

Valproate, ethosuximide Valproate

Lamotrigine Lamotrigine

Carbamazepine, valproate

Etc

(lamotrigine

most effective, slow

titration)

*

Common S/E all may cause drowsiness and rash

o

o

o

ValproateWeight gainHair lossRare idiosyncratic liver failure

CarbamazepineRashNeutropeniaHyponatraemiaAtaxiaLiver enzyme induction

Lamotigineo

*

Rash

Benzo'sSedationToleranceIncreased secretions

Other Treatments

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