Chapter 11: NEUROLOGICAL DISORDERS
Student Authors: Farai Chigumadzi and Peter Aclavio
Specialist Advisor: Dr Chantel Richardson
This chapter covers the following topics:
- Non-accidental injury (NAI)
- Acute flaccid paralysis (ASD)
- Autism Spectrum Disorder(ASD)
- Temper tantrums
- Night terrors
- Breath-holding attacks
- Enuresis
- Encopresis
- Microcephaly
- Hydrocephalus
- Movement disorders
- Seizure disorders
- Paediatric stroke
- Headache
- Myelomeningocoele/meningomyelocoele
- Meningitis
- Spinal muscular atrophy (SMA)
- Neurocutaneous syndromes
- Cerebral Palsy
NON-ACCIDENTAL INJURY (NAI)
It is a common problem and can be potentially life-threatening. Healthcare professionals have a duty to report any suspected or confirmed NAI to the relevant authorities e.g. senior clinical staff or child protection services.
Aetiology
NAI may be the result of maltreatment in the form of:
- Physical abuse
- Neglect
- Sexual assault
- Psychological abuse
- Medical abuse
Clinical Features
The child may present with:
- Pain
- Swelling
- Bruising
- Limping
Below (table 11.1) are some red flags which may indicate that the child has suffered an NAI:
Table 11.1: NAI Red Flags
Red Flags on History | Red Flags on Examination |
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Investigations
They should include
- Skeletal survey (X-rays)
- CT scan
- Ophthalmologic assessment
Management
One must carefully record the child’s injuries and contact the relevant authorities e.g. child protection services, senior staff, police.
ACUTE FLACCID PARALYSIS (AFP)
It is a clinical syndrome characterised by the rapid onset of weakness and reduced muscle tone without an obvious cause. Early diagnosis improves both morbidity and mortality.
Pathophysiology
The syndrome is the result of anterior horn cell injury which is usually secondary to viral infection (e.g. polio; however polio has nearly been completely eradicated) or immune-mediated peripheral pathologies.
Aetiology, Clinical Features and Investigations
Guillain Barré syndrome (GBS) is the most common cause of AFP in SA. It is classically preceded by a URTI and is characterised by symmetrical motor weakness of the lower limbs which ascends to involve the trunk and upper limbs to varying degrees. Fortunately, 80% of patients make a full recovery. Pertinent clinical signs include:
- Weakness of the limbs, face, bulbar muscles and respiratory muscles
- Reduced or absent reflexes
- Sensory loss in a glove and stocking pattern of distribution
- Autonomic instability (unstable BP, irregular HR, urinary incontinence)
An LP should be done as it will show isolated raised CSF protein in GBS and can be used to exclude other causes.
Management
One’s immediate management priorities are to diagnose the child with AFP and provide:
- Supportive management
- Monitoring of respiratory status
- Physiotherapy and occupational therapy (indicated in immobile children; help improve functioning)
IV gamma globulin is also used.
AUTISM SPECTRUM DISORDER (ASD)
See the Disorders of Development chapter
TEMPER TANTRUMS
They are unpleasant and disruptive behaviours and emotional outbursts. They may be common in some communities and usually manifest between the ages of 15 months and 3 years.
Temper tantrums are associated with unmet needs or desires i.e. the child is not allowed to ‘have his/her own way’. They form part of the ‘negative stage of child development’ and are worsened by the child’s lack of vocabulary to fully express their feelings.
Clinical Features
Generally, the parent will give a history of the child lying down, kicking and screaming. The physical exam will be normal and is only done to reassure the parent.
Red flags include:
- Tantrums which worsen after 4 years of age (see related image here)
- Self-injury or damaging of property during the tantrum
- Breath-holding (especially if the child faints)
- Developmental regression
- Refusal to eat or sleep
- Headaches
- Development of anxiety
Management
Temper tantrums are usually a passing phase and these children generally respond well to counselling. Parents must be reassured and given encouragement. They should not reinforce the negative behaviour by acquiescing to the child, but need to be taught coping strategies. Principles of management include:
- Offering alternatives to the desired object or activity to avoid frustrating situations
- Ignoring or walking away from the child
- Not punishing the child (do not hit or argue with the child)
- Showing approval and giving attention when the child displays positive or acceptable behaviour
- Maintaining consistency
Problems occur when parental control is lacking or the family has a chaotic lifestyle. Important factors to consider when managing these patients are:
- Child’s temperament
- Parent’s temperament
- Inconsistency of the parent’s behaviour towards the child
NIGHT TERRORS
This term refers to episodes when the child suddenly wakes up at night and is very upset.
Clinical Features
Night terrors generally occur during phase 3 non-REM (deep) sleep and usually occur early in the night. The episode tends to last 10-20 minutes and the child usually has 2-3 episodes weekly. Clinical features include:
- Screaming and jumping out of bed as if running away from something scary
- Hitting in all directions
- Having eyes wide open
- Disorientation on waking
- Failure to recognise someone who is trying to help him/her
- Failure to remember the episode the next day
Management
There is no specific treatment for night terrors. The child cannot be soothed during the episode but s/he will fall asleep after an episode. One must not try to wake the child.
If the night terrors take place at the same time every night, the child can be woken up 15 minutes before the time to try and prevent the episode. The child is then allowed to stay awake for a few minutes before falling asleep again.
BREATH-HOLDING ATTACKS
They are closely related to temper tantrums and are usually present between the ages of 6 and 18 months (rare in children >4 years).
Classification and Clinical Features
Breath-holding attacks may be of the cyanotic- or pale-type. Anoxia precipitates both types of attack and both types are associated with iron-deficiency anaemia.
- Cyanotic-type:
- It is more common and is associated with temper tantrums. Episodes typically last 10-30 seconds.
- The child’s crying turns into hyperventilating and the child may become apnoeic and cyanosed. The child may even develop increased limb tone or clonic movements.
- These clinical features cease when the child starts breathing normally. S/he will be apathetic but fully conscious afterwards.
- Pale-type:
- It is associated with minor injury or fear.
- The child develops severe pallor, bradycardia and may, in some instances, become asystolic (due to increased vagal tone).
Management
The parents must be reassured that the condition is benign and is unrelated to epilepsy. However, a full history must be done and thorough physical examination done. Iron-deficiency should also be corrected, if present.
ENURESIS
See the Child and Adolescent Psychiatry chapter.
ENCOPRESIS
See the Child and Adolescent Psychiatry chapter.
MICROCEPHALY
It is defined as an abnormally small head (head circumference >2 standard deviations below normal. Microcephaly (see related image here) may be isolated or 219 may be associated with congenital anomalies. It is a disorder of cell proliferation and brain growth as a whole is defective. The frontal lobes are usually more affected following perinatal insults. The cerebellum is usually relatively spared.
Aetiology
Causes of microcephaly include:
- Normal variant
- Hypoxic ischaemic encephalopathy (most common cause)
- Foetal alcohol syndrome (FAS) – see related features here
- Infections:
- Toxoplasmosis
- CMV
- Zika virus
- Intrauterine growth restriction
- Inborn errors of metabolism
- Other genetic conditions
Clinical Features
The child may present with:
- Neurodevelopmental delay
- Hearing or vision problems
- Epilepsy
- Cerebral palsy
Management
No treatment is available to reverse microcephaly. Parents should be counselled and individual problems treated by the multidisciplinary team, such as audiology referral to manage for hearing impairment, and occupational therapist referral to teach the child skills which help him/her better integrate into society. Anticonvulsants may be prescribed for the child with seizures.
HYDROCEPHALUS
It is an abnormally large head with an increased CSF volume and/or pressure.
Pathophysiology
Hydrocephalus is the result of:
- Obstruction of CSF flow
- Overproduction of CSF
- Decreased absorption of CSF
Aetiology
Hydrocephalus may be caused by:
- Infection e.g. TB, other causes of meningitis
- Genetic factors
- Malignancy (rare)
- Trauma
- Congenital disease e.g. aqueduct stenosis, Arnold-Chiari Malformations
See related image here.
Clinical Features
The child may present with:
- Macrocephaly (diagnosed at birth or antenatally)
- Setting-sun eyes
- Bulging fontanelles
- Anorexia
- Vomiting
- Irritability
- Lethargy
Management
Serial head circumference measurements should be taken and plotted to track progression. The child should be referred early for the insertion of a shunt 221 (ventriculoperitoneal shunt or third ventriculostomy). Once a shunt has been placed, the child must be regularly followed up to ensure that it has been correctly inserted.
MOVEMENT DISORDERS
They include:
- Ataxia
- Chorea
- Dystonia
- Athetosis:
- This term refers to slow, writing movements of limbs.
- It may occur in patients with chorea or hypoxic ischaemic encephalopathy resulting in cerebral palsy.
- Tics (see Child and Adolescent Psychiatry chapter)
- Tremor:
- A tremor is an involuntary, oscillatory movement with a fixed frequency.
- One must exclude hypothyroidism.
- Myoclonus:
- These rapid muscle jerks have decreased frequency and severity when the patient is asleep.
- However, unlike tics, they do not disappear in sleep.
Ataxia
It is unco-ordination of postural control and gait, as well as unco-ordination of skilled movements involved in fine hand movements and speech.
Aetiology
Disturbances in cerebellar function generally lead to ataxia. One must be able to differentiate acute causes from chronic conditions.
- Acute causes:
- Infection:
- Viruses (which cause meningitis) e.g. VZV, coxsackie virus, Epstein-Barr virus, influenza, mumps, measles
- Bacteria (which cause meningitis or cerebral abscesses) e.g. diphtheria, pertussis, typhoid, scarlet fever
- Alcohol
- Toxins or metabolic disease e.g. hypoglycaemia, lead, glue, mercury
- Drugs e.g. phenytoin, carbamazepine, phenobarbitone
- Posterior fossa tumours
- Trauma (cerebellar haemorrhage)
- Basilar migraine
- Pseudo-ataxia (non-convulsive status epilepticus)
- Chronic causes may be perinatal or postnatal
Table 11.2: Perinatal and Postnatal Causes of Ataxia
Perinatal Causes | Postnatal Causes |
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Clinical Features
The cerebellum matures with age, therefore signs which are considered pathological in the adult may be physiological in the child. Clinical features may include:
- Truncal ataxia – poor posture, exaggerated joint angles, head lag, truncal hypotonia
- Volitional ataxia – dysmetria, dysdiadochokinesia, nystagmus, dysarthria, staccato speech
- Hypotonia
Chorea
Choreas are rapid, brief, jerky movements that are irregular and unpredictable. They are often associated with hypotonia. It is thought that the caudate nucleus and subthalamic nuclei are involved in the pathophysiology of chorea. One must always consider rheumatic fever as a cause of the chorea (Sydenham’s chorea).
Sydenham’s Chorea
It is characterised by abrupt, irregular and purposeless movements. ARF is the most common cause of acquired chorea in the young (see Cardiovascular Diseases chapter). Sydenham’s chorea is common in the developing world.
Clinical Presentation
This major manifestation of ARF is characterised by:
- Insidious onset (4 months post initial infection)
- Migratory chorea
- Hypotonia
- Emotional lability
- Fidgeting
Management
One must investigate to exclude cardiac pathology. All affected children should be given penicillin V followed by prophylaxis, if ASOT titres and anti-DNAse levels are raised. The chorea is treated with the lowest-tolerated dose of haloperidol (see related image here) or with sodium valproate. The child should be referred to a paediatrician if his/her activities of daily living have been affected.
Dystonia
It is simultaneous, sustained contraction of agonist and antagonist muscles, leading to posture disturbances and involuntary movements of the trunk, limbs and face. These movements are slow, laboured and repetitive in nature (alternate between flexion and extension).
It may be caused by:
- Drugs e.g. haloperidol, metoclopramide
- Bilirubin encephalopathy:
- Severe neonatal jaundice leads to the deposition of bilirubin in the basal ganglia (will see kernicterus on pathological examination).
- These children often present with dyskinetic movements.
SEIZURE DISORDERS
Seizures are caused by abnormal and excessive neuronal activity in the brain, and lead to transient signs and symptoms
Aetiology
Seizures may be caused by:
- Infection
- Hypoxia during gestation and/or after birth
- Intracranial haemorrhage
- Hypoglycaemia
- Drug withdrawal
- Developmental abnormalities
Diagnosis and Investigations
A seizure disorder may be diagnosed if the child has had >2 unprovoked seizures. However, a thorough and reliable history is very important, especially eyewitness reports (video footage can be very helpful). Other investigations which may be helpful include:
- Brain MRI (to look for lesions in the brain which may be causing the seizures)
- Electroencephalogram (EEG; can be used to rule-in seizures but cannot be used to rule them out)
See related image here.
Classification and Clinical Features
Seizure disorders may be classified into syndromes based on clinical features:
- Generalized seizures e.g. tonic-clonic, myoclonic, absence, atonic
- Focal seizures
- Other e.g. neonatal seizures
- Neonatal seizures are subtle – due to relatively underdeveloped cortex
- Facial grimacing, nystagmus, sudden loss of time, eye blinking and chewing
Febrile Seizures
They are generalised seizures which occur because of an extracranial cause of fever. They affect children aged 6 months to 5 years and do not usually last longer than 15 minutes. There is often a family history of febrile seizures.
Classification
There are two categories of febrile seizures:
- Simple febrile seizures:
- They are generalised seizures which last <15 mins and do not recur within a 24-hour period.
- They are most commonly generalised tonic-clonic seizures.
- Complex febrile seizures:
- They have a focal onset, last >15 mins and recur within 24 hours
Infantile Spasms
They mainly occur in children within the first year of life and are characterised by
- Epileptic spasms (flexor, extensor or mixed flexor-extensor spasms)
- Hypsarrhythmia on EEG
Aetiology
Causes of infantile spasms include:
- Neurocutaneous syndromes e.g. tuberous sclerosis
- Hypoxia
- Infections
- Trauma
- Hypoglycaemia
- Inborn errors of metabolism
When the diagnosis of infantile spasms is made, one must assess the child for West syndrome. West syndrome is diagnosed based on the presence of the following triad:
- Flexor or extensor spasms
- Hypsarrhythmia on EEG
- Mental retardation
Management
Infantile spasms are a neurological emergency, therefore an EEG must be urgently done. However, they are strongly resistant to conventional anti-epileptic treatment. The treatment of choice is with a combination of steroids and vigabatrin. Vigabatrin alone may be given to patients with tuberous sclerosis.
Table 11.3: Status Epilepticus
Status Epilepticus
It is an epileptic seizure which is sufficiently long or regularly repeated to produce a varying and enduring epileptic condition, in terms of convulsions or mental state i.e. the child has seizures lasting 30 mins or longer with no recovery of consciousness between seizures. Status epilepticus is common in the first two years of life.
General Management of Seizures
The aim of management is to maintain vital functions. Thus, one must identify the cause and treat it according to the relevant protocol.
General management principles include:
- Attempting to control symptoms with monotherapy (although resistant forms may need 2 or 3 anticonvulsants before control is gained)
- Gradually titrating up doses of new anticonvulsants (weekly)
- Monitoring the child for side effects
If one is unable to control seizures with the correct agent that is being given at the appropriate dose, the child should be referred to a paediatrician or paediatric neurologist.
Non-specialist management options may be grouped according to seizure type:
- Generalised or focal seizures – phenobarbitone, phenytoin (only use for status epilepticus in children), carbamazepine, sodium valproate
- Absence seizures – sodium valproate, ethosuximide
- Complex partial or focal seizures – carbamazepine, phenytoin
- Febrile seizures – diazepam (phenobarbitone and sodium valproate are seldom used for febrile seizures)
- Myoclonic seizures – sodium valproate, clonazepam
PAEDIATRIC STROKE
It may occur in a child with any of the following risk factors:
- Inflammation or infection e.g. meningitis (bacterial or mycobacterial), HIV
- Cardiac disease
- Haematological or thrombotic syndromes/
Classification
Paediatric strokes may be classified according to
- Lesion type (haemorrhagic or ischaemic)
- Vessel type (arterial vs venous)
If the stroke is arterial, it may be further classified as embolic or thrombotic.
Aetiology
An ischaemic stroke may be the result of:
- Vascular disease:
- Vasculopathies e.g. focal cerebral arteriopathy (may occur post-VZV infection)
- Vasculitides e.g. meningitis, Takayasu’s arteritis
- Intravascular disease:
- Haematological conditions e.g. sickle cell, leukaemia, polycythaemia
- Prothrombotic state, which may be due to:
- Congenital conditions e.g. protein C or S deficiency, factor V Leiden mutations
- Metabolic disease e.g. hyperlipidaemia, homocysteinaemia
- Embolic cause:
- Congenital heart disease
- Acquired heart disease e.g. rheumatic heart disease, infective endocarditis, prosthetic heart valve
A haemorrhagic stroke may be the result of:
- Vascular disease:
- Congenital vascular anomalies e.g. arteriovenous malformation, venous angioma, cavernous malformation, intracranial aneurysm
- Vasculopathies e.g. moyamoya disease, connective tissue disorders, sickle cell disease
- Intravascular disease (haematological disorders):
- Idiopathic thrombocytopenic purpura (ITP)
- Thrombotic thrombocytopenic purpura
- Haemophilic states
- Clotting factor deficiencies
- Liver dysfunction
- Vitamin K deficiency
Clinical Features
The child will present with a specific stroke syndrome based on the artery involved:
- Internal carotid artery:
- Hemiplegia
- Hemianopia
- Aphasia (if the dominant hemisphere is affected)
- Middle cerebral artery (MCA):
- Hemiplegia (arm and face are more affected than leg)
- Hemianopia
- Aphasia (if the dominant hemisphere is affected)
- Anterior cerebral artery (ACA):
- Hemiplegia (leg is more affected than arm or face)
- Posterior cerebral artery (PCA):
- Hemiparesis
- Homonymous hemianopia
- Ataxia
- Vertigo
- Penetrating branches:
- Pure motor involvement
- Pure sensory involvement
- Sensorimotor involvement
- Speech involvement (occasional)
Approach
History
The child may present with:
- Sudden onset of neurological deficit (suggestive of an embolic event)
- Gradual onset of neurological deficit (suggestive of an arteriopathy or thrombotic event)
- History of recent illness (e.g. chicken pox) or trauma to the head
- Family history of young strokes
Examination
One must pay look for attention to:
- Changes in GCS
- Evidence of raised intracranial pressure
- Evidence of meningitis
- Neurological deficits (including aphasia/dysphasia)
- Evidence of bleeding abnormality or vasculitis
- Cardiovascular disease
Investigations
They should include:
- Blood tests:
- FBC and differential count
- ESR
- Infection screen (HIV, TB, VZV, toxoplasma)
- Hb electrophoresis (dependent on ethnic group)
- Fasting lipogram
- Lupus screen
- LP (to assess CSF for infection)
- Imaging:
- CT (to exclude haemorrhage and define the territory involved)
- MRI and magnetic resonance angiography (MRA)
- Conventional angiography
Differential Diagnoses
Paediatric stroke mimics include:
- Seizures and epilepsy (Todd’s paresis)
- Migraine
- Psychogenic disease
- Inflammatory disease
- Intracranial infections
- Metabolic causes
Management
The aim of acute management is to preserve the penumbra. This is done by:
- Maintaining a low-to-normal body temperature
- Ensuring euglycaemia
- Maintaining good oxygen saturation
- Ensuring adequate cerebral perfusion
Secondary prevention should be started in patients with underlying cardiovascular disease. Start the child on anticoagulation with low molecular weight heparin. It is recommended that these children are managed in consultation with the relevant specialist (paediatric neurologist, haematologist or cardiologist).
Rehabilitation is multidisciplinary and should involve a physiotherapist, occupational therapist, audiologist and speech therapist. One must address issues with feeding, nutrition, pain, communication, mobility and positioning.
HEADACHES
Headaches are common in children and their frequency increases with age. Most headaches are benign. However, one must take a detailed history of the pain (SOCRATES) and ask about social and psychological factors.
Aetiology
Headaches may be caused by:
- Primary headache syndromes:
- Migraine
- Tension headache
- Secondary headache syndromes:
- Sinusitis
- Meningitis
- Encephalitis
- Hydrocephalus
- Sleep apnoea or hypoventilation
- Benign intracranial hypertension
- Haematoma
- Brain abscess
- Brain tumour
Approach
One must rule out pathological causes of headaches by asking about the following danger signs:
- Headache which interrupts sleep
- Headache present on waking
- Visual disturbances
- Altered level of consciousness
- Focal neurological deficits
- Hypertension
If any of the above features are present, one must investigate further with:
- Lumbar puncture (to exclude meningitis)
- CT scan
Patients with danger signs and who cannot be managed at the primary care level should be referred to a paediatrician or paediatric neurologist.
MYELOMENINGOCOELE/MYELOMENINGOCOELE
A myelomeningocoele (see related image here) is a midline defect of the skin and vertebral arch which contains both meninges and neural tissue. The lumbosacral region of the spinal cord is the most commonly affected area. One must look for sensorimotor impairment as well as bladder and bowel incontinence.
Aetiology
The aetiology of myelomeningocoeles is poorly understood. However, evidence suggests that there is an association with inadequate levels of folate before conception and during the first trimester. There is an increased risk of recurrence in subsequent pregnancies.
Arnold-Chiari malformations are the most commonly associated congenital anomalies (lead to hydrocephalus).
Diagnosis and Investigations
Myelomeningocoeles may be diagnosed:
- In-utero via ultrasound (termination may be offered at this point)
- At birth
Once diagnosed, one should perform a CT scan and cranial USS (to assess initial ventricular size so that subsequent monitoring can be done).
Management
Prenatal counselling should
- Prenatal counselling
One should attempt to diagnose the condition early – in-utero or at birth. If diagnosed in-utero, prenatal counselling should be performed. If diagnosed at birth, one should initiate emergency management:
- Keep the defect and tissues sterile and moist (place saline-soaked gauze over the defect)
- Refer the child for urgent surgical correction (within 48 hours of delivery)
233 Associated abnormalities must then be excluded. A multidisciplinary team must be involved in the care of this child (neurologist, orthopaedic surgeon/neurosurgeon, physiotherapist, urologist).
MENINGITIS
See Infectious Diseases chapter.
SPINAL MUSCULAR ATROPHY (SMA)
It is an autosomal recessive disorder which is characterised by progressive hypotonia and muscular weakness. It is a common genetic cause of mortality in children, with males being affected more commonly than females (2:1). There is a high prevalence in Central and Eastern Europe.
Pathophysiology
The primary pathology involves progressive degeneration of 𝛼𝛼-motor neurons on anterior horn cells in the spinal cord. This is caused by a mutation in the gene responsible for the survival of motor neurons.
Clinical Presentation
The child will present with:
- Abnormal posture (pronated arms)
- Proximal weakness with atrophy
- Cranial nerve involvement, especially bulbar signs (in some patients) e.g. tongue fasciculations
- Reduced tone
- Areflexia
- Bell-shaped chest
- Normal sensation
- Normal intelligence
- Sparing of involuntary muscles (heart, sphincters, GIT)
Classification
SMA is classified into four types according to the age of onset of clinical features and most advanced physical milestone achieved:
- Type 1 – the children typically present within the first six months of life; they are unable to sit unsupported
- Type 2 – the children typically present at 3-15 months old; they are able to sit without support but are never able to stand or walk
- Type 3 – the children typically present between 18 months old and adulthood; they achieve independent ambulation
- Type 4 – the patient presents after 30 years of age (latest onset disease); all motor milestones have been achieved and independent ambulation is usually maintained through life
The prognosis is worse the younger the age of onset is. The median age of death is 10 years old and is normally due to respiratory compromise.
Management
Children with SMA are all affected differently, therefore treatment should be catered to the individual. Management is mainly supportive and involves a multidisciplinary team (pulmonologist, orthopaedic surgeon, nutritionist, genetic counsellor, social worker, occupational therapist, physiotherapist and orthotist). Surgical interventions are considered to treat scoliosis, contractures and fractures.
Thus far, no cure has been found but research is ongoing. Currently, scientists are looking at inhibitors of GABA synthesis and genetic therapy which attempts to fix/replace the affected gene.
NEUROCUTANEOUS SYNDROMES
They are congenital disorders that are due to genetic changes. Tissues and organs derived from the ectoderm are generally affected (i.e. skin, nervous tissue, eyeballs and retina), however bones and visceral organs may also be affected. The conditions evolve slowly throughout childhood and the lesions have malignant potential.
Diagnosis
Neurocutaneous syndromes may be diagnosed based on the results of:
- Genetic tests
- MRI scan
- CT scan
- EEG
- Eye exam
- Lesion biopsy
Classification
Neurocutaneous syndromes include:
- Tuberous sclerosis
- Sturge-Weber syndrome
- Neurofibromatosis
Tuberous Sclerosis
It is an autosomal dominant with variable expression. Features evolve as the child grows. It is diagnosed based on the presence of two major features, or one major feature and two minor features. TSC1 gene mutations are familial and TSC2 gene mutations are associated with adult polycystic kidney disease.
Sturge-Weber Syndrome
In this syndrome angiomas cross the leptomeninges and involve the skin of the face, producing a characteristic skin lesion (typically in the ophthalmic or maxillary region of the trigeminal nerve). The associated mutation is sporadic and there are three subtypes of the syndrome.
Affected children may present with:
- Facial naevus (port wine stain)
- Seizures
- Hemiparesis
- Hemianopia
- Headaches
- Glaucoma
- Learning difficulties
- Developmental delay
Neurofibromatosis (NF)
There are two types – NF 1 and 2. Males and females are equally affected (1:1) in both types (see related image here).
Neurofibromatosis Type 1 (Nf1)/Von Recklinghausen’s Disease
This is an autosomal dominant condition which is more common than NF2. The child may present with:
- Cafe-au-lait spots
- Benign tumours – neurofibromas (see image linked above)
- Lisch nodules
- Seizures
- Scoliosis
- Facial pain
- Numbness
- Variable degree of intellectual disability
- Attention deficit disorder
NF1 is diagnosed based on the presence of specific diagnostic criteria:
- First-degree relative with confirmed NF1
- ≥6 café-au-lait spots
- Neurofibromas
- Optic glioma
- Axillary freckling
- Lisch nodules
- Bone lesions e.g. sphenoid dysplasia
Neurofibromatosis Type 2 (Nf2)
The child may present with:
- Hearing loss (due to vestibular schwannomas)
- Meningiomas
- Spinal tumours
- Neuropathies
- Headaches
- Facial pain
- Problems with balance and walking
- Neurofibromas
- Café-au-lait spots
Management
There is no cure for neurocutaneous syndromes. Management depends on the individual child’s needs and requires input from a multidisciplinary team:
- Paediatric neurologist
- Plastic surgeons
- Genetic counsellor
- Neurosurgeon
- Ophthalmologist
- Dermatologist
- Oncologist
- Occupational therapist
- Speech therapist
- Physiotherapist
CEREBRAL PALSY
See Disorders of Development chapter.