Narakas Group	Roots and Muscles Affected	Outcome
Group 1	C5, C6. Biceps and deltoid	90% recover fully
Group 2	C5, C6, C7. All except long finger flexors	65% recover fully; the rest have permanent deficit
Group 3	C5, C6, C7, C8, T1. All except slight finger flexion	1–2% recover fully; the rest have significant permanent deficit
Group 4	C5, C6, C7, C8, T1 and Horner’s. All muscles and sympathetic function	None recovers fully; all have severe permanent deficit

Failure of biceps recovery by 4 months also heralds a poor result.

Initial treatment is with physiotherapy to prevent joint contractures due to muscle imbalance. In group 4 cases with no biceps recovery by 4–6 months, nerve repair by grafting or nerve transfers may restore useful, but never good, function. Partial recovery produces muscle imbalance, particularly at the shoulder, which limits function and may cause dislocation of the shoulder. Surgery to weaken the internal rotators or muscle transfers to strengthen the external rotators prevents dislocation and improves function. Muscle transfers can also help residual wrist or hand weakness.

Paediatric foot and ankle

Definitions of position and deformity

The hindfoot (talus and calcaneus) is described as valgus if it deviates laterally, varus if deviation is medial. When the tilt is subtalar, involving the heel, the terms eversion and inversion correspond. As with the hand, the midfoot and forefoot are said to pronate when they roll internally, often in conjunction with eversion of the heel, and to supinate when they roll externally with the first metatarsal raised above the fifth and the heel inverted. Similarly, medial deviation of the forefoot (metatarsals and toes) in the horizontal plane is adduction, the opposite being abduction. Dorsiflexion of the foot normally occurs as a total movement, but may be confined to the heel alone, as with the deformity ‘calcaneus’ seen with a weak calf after poliomyelitis and other neurological conditions, including some forms of pes cavus. Equinus describes the toe-down position of the whole foot or the heel, but when only the midfoot and forefoot are plantar-flexed the term used is ‘plantaris’.

The arch of the foot is maintained by the conforming shape of the bones, ligaments and muscles, both intrinsic and from the calf. Maintenance of this medial or longitudinal arch is reliant upon normal muscle action, especially at push-off when walking. A transverse metatarsal arch is also present, although it is less obviously so; in the elderly this arch may be lost along with flattening of the medial arch as the weakening foot pronates.

Presentation of foot deformities at different ages

Birth

At birth, during infancy and when the child is a toddler, variations from normal may be encountered (see Chapter 24).

Metatarsus adductus

This appearance is relatively common and usually benign. Provided the forefoot alignment is correctable and there is no element of supination, the condition can be ignored and will lessen during the early years of shoe-wear. Hallux varus or adductus is highly unusual; this congenital condition may require soft-tissue correction later in childhood.

Congenital talipes equinovarus (clubfoot or congenitally inverted foot)

This is the most common significant deformity of the foot encountered at birth (Fig. 25.3). It is more likely to occur in boys. A family history is often identified, reaching its peak with identical twins when the condition is seen in 33% of siblings. Milder forms of the deformity may result from tight uterine ‘packaging’, including oligo-hydramnios. The more structurally severe feet have been shown to have neurological, vascular and other soft-tissue abnormalities.

FIGURE 25.3 Congenital talipes equinovarus (clubfoot). (A) In the infant; (B) as an established deformity in childhood

The prognosis for clubfoot is related to the severity of the presenting deformity, graded from postural to mild, moderate or severe. Atypical syndromic clubfeet are also encountered: the deformities may be very stiff in conditions, such as arthrogryposis, or they may correct more rapidly than the idiopathic forms, potentially leading to over-correction if surgery is undertaken.

The current management of a newly presenting idiopathic club foot is by the Ponseti method. This involves a programme of carefully applied plaster casts that gradually correct the deformity. This usually offers excellent correction of the deformity but about 30% of babies will also require a percutaneous Achilles tenotomy (division) to correct residual hindfoot equinus. The correction is then maintained by the child wearing a foot abduction splint at night until approximately 2–4 years of age.

Surgery is reserved for feet that have relapsed or for those presenting late where there is fixed skeletal deformity.

Childhood

Osteochondritic conditions

These affect the navicular (Kohler’s disease) in mid-childhood and the second or occasionally other metatarsal heads (Frieberg’s disease) in early adolescence. The former resolves completely, although a strong shoe with an insole, or plaster cast support for a month or two, may be helpful if it is symptomatic. Frieberg’s disease leads to pain in the affected metatarsophalangeal (MTP) joint and a tender enlargement of the metatarsal head. An extension osteotomy of the metatarsal neck may relieve metatarsalgia, although the dorsal bony swelling persists. The long-term outcome of this condition, when healed, is poorly recorded.

Pes cavus

A high longitudinal arch is rarely a problem in early childhood, but becomes increasingly symptomatic towards the later stages of skeletal growth. Four principal patterns of neurological imbalance produce these chronic changes in the foot:

1. Weakness of soleus and gastrocnemius, with over-action of the long toe flexors

2. Weakness of ankle dorsiflexion resulting in over-action of the long toe extensors

3. Weakness of the intrinsic muscles

4. A weak peroneus brevis muscle with overactive peroneus longus.

The neurological conditions responsible include cerebral palsy, poliomyelitis, Friedreich’s ataxia, myelomeningocele and other abnormalities of the spinal cord, such as spinal dysraphism or syringomyelia, and peripheral neuropathies. The commonest cause of this in the UK is hereditary sensory and motor neuropathy (HSMN) type 1 (Charcot–Marie–Tooth disorder or peroneal muscular atrophy; see also Chapter 26). This autosomal dominant progressive local demyelinating disorder produces an initially correctible and then a rigid deformity associated with painful calluses. Hammering of the toes and hindfoot varus are also present.

Clinical assessment should include neurological examination (loss of light touch, vibration or proprioception; diminished deep reflexes; ataxia and dysarthria; clonus and overt muscle wasting).

When further investigation is warranted, X-rays of the feet and magnetic resonance imaging (MRI) of the spine are indicated. Imaging of the brain and spinal cord may also be necessary, and both nerve conduction studies and electromyography are helpful in ruling out overt nerve deficit. In many cases no underlying cause is found.

Treatment consists of:

• Soft-tissue surgery (releases and tendon transfers)

• Osteotomies (first metatarsal, midfoot, calcaneum)

• Triple arthrodesis of the talus, calcaneum and cuboid.

The toes are often clawed, requiring flexor tendon releases or tendon transfers. Orthoses will help to reduce local pressure over the metatarsal heads.

Tiptoe walking

This gait pattern may develop at walking age or a little later in childhood. In some cases this is due to mild spastic diplegia (see also Chapter 26). The majority of children with the condition seem to be neurologically normal, so the term ‘tight heel cords’ or ‘ballerina syndrome’ is used. Stretching by physiotherapy or casting is usually effective, but may have to be repeated. Lengthening of the Achilles tendon is avoided whenever possible because it is the calf muscle rather than the tendon that is pathologically shortened.