confusion/delirium
loss of communication
dysphagia
seizures
nausea/vomiting
spasticity
dyspnoea
immobility
constipation depression
fear anxiety
stigma/guilt loss of income
fear for children spouse & dependants religious
non religious
why me?

MAIN SYMPTOMS

Pain

Pain is defined as a subjective unpleasant sensory and emotional experience associated with actual or potential tissue damage. Pain is a common disorder and WHO estimates that 5-30% of the world’s population experience persistent pain depending on where they live. The most commonly affected sites worldwide are head, neck, knees and lower back. Pain is influenced by the patient’s mood, morale and the underlying reason for the pain. Chronic pain may persist long after the tissue damage has been done and is defined as pain lasting for >3/12.

Total pain is an interaction of the physical, emotional, psychological and spiritual components. The consequences of pain include immobility, depression, poor sleep and nutrition and overdependence on family and carers. Longer term consequences affect employment, family, and social life. Chronic pain as a result of neurological disorders is a major and neglected cause of disability in Africa. The management of pain involves non pharmacological measures, drug treatments, psychological and spiritual support. The aim of drug treatment is to provide an effective and regular treatment which completely stops pain and prevents its recurrence. The commonly used drugs in pain control (Table 20.4) and the WHO steps in their use (Table 20.5) are outlined below.

Pathophysiology

Pain is broadly classified into two types: nociceptive and neuropathic (Table 20.2). The difference between nociceptive and neuropathic is not always clear-cut clinically and any one individual may suffer from one or both types of pain.

Nociceptive pain is caused by activation of primary pain receptors in tissues and is transmitted to the brain through slow non myelinated peripheral C fibres and faster conducting larger myelinated (A) fibres. It can be either somatic arising from skin, musculoskeletal (muscle spasticity, joint deformities) or visceral arising from internal organs (malignancy, stone) or bone (fracture). The type of pain depends on the site, origin and cause of pain. It ranges from the familiar pricking and burning pain in skin conditions to a dull, continuous, diffuse, aching as described in internal malignancy or the intermittent, sharp and colicky pain which occurs in gastrointestinal or ureteric colic.

Neuropathic pain by contrast is mostly neurological in origin arising from damaged neural tissue either in the peripheral or the central nervous system. The main sites of origin are peripheral nerves (HIV, diabetes), nerve roots (herniated disc, herpes zoster), spinal cord (paraplegia) and the brain (post stroke). The sensations that characterize neuropathic pain are variable and often multiple and are described as burning, gnawing, aching or lancinating (knife-like) or shooting in character. There is frequently numbness or dysaesthesia (altered unpleasant sensation) or allodynia (when a non painful stimulus is perceived as pain) in a superficial sensory distribution coupled with local autonomic dysfunction. Neuropathic pain can be either intermittent, lasting seconds or continuous, lasting hours, and can persist even without the stimulus. It generally responds poorly to treatment. Pain without identifiable tissue or nerve damage is termed idiopathic. The N-methyl–D aspartate (NMDA) channel receptor complex, substance P, bradykinin and serotonin are all involved in the pathophysiology of pain. These are found predominantly in the spinal cord and peripheral nervous system.

Measurement

All types of pain should be described fully in terms of quality, severity, location, mode of onset, provoking and relieving factors, and time course. Pain is subjective but can be measured. The simplest measurement uses self reported severity in terms of mild, moderate, severe and very severe which can be recorded and graded on a corresponding scale of 1-4. In clinical practice however, there is widespread use of the verbal or written analogue scale. This is a scale of 1-10, where 1 is the least and 10 is the worst pain imaginable. The patient is asked ”where on this scale of 1-10 do you put your pain?” The value of the pain scale is that it is independent of language, easy to understand and use and can be recorded and repeated at each patient visit and response to therapy monitored.

Major causes of neurological pain in Africa

MANAGEMENT OF PAIN

Relief of pain should be the responsibility of all health care workers. The main aim is to diagnose, treat and stop the pain. In chronic neurological disorders this frequently involves providing maximal pain relief, as complete alleviation is not always possible. The range of clinical treatments includes non pharmacological and pharmacological measures. The non pharmacological approach is summarised in Table 20.3. The drug treatment of pain of neurological origin is based on the distinction between the pain of nociceptive and neuropathic origin and is summarised in Table 20.4 In practice, although these may be difficult to distinguish, the pain of nociceptive origin responds better to non-opioid analgesics such as paracetamol, aspirin and non steroidal anti-inflammatory drugs whereas pain of neuropathic origin responds best to tricyclic antidepressants e.g. amitriptyline and the anticonvulsants e.g. gabapentin and carbamazepine. Opioids can be used in both types and their role in the management of pain is summarized below in Table 20.4. Pain due to local compression of peripheral nerves or nerve roots may be relieved by appropriate surgery. Nerve root blocks and epidural spinals provide temporary relief. Patients with chronic pain benefit from a multidisciplinary approach involving cognitive behaviour therapy, physiotherapy and occupational therapy.

DRUG TREATMENT OF PAIN

Non-opioids

These include non steroidal anti-inflammatory drugs (NSAIDs) and paracetamol. The most commonly used NSAIDs are aspirin, ibuprofen, and diclofenac. Their doses, routes of administration and side effects are outlined in Table 20.4. These are the main first line treatment for most pain regardless of whether it is of nociceptive or neuropathic origin and are used at all 3 steps in the WHO analgesic ladder (Table 20.5). NSAIDs should be used cautiously in patients with renal impairment as they may further impair function and may provoke renal failure. In patients with a history of dyspepsia the concurrent prescription of proton pump inhibitors or histamine-2 receptor blockers help to reduce the symptomatic upper GIT side effects.

Opioids

Opioids include all drugs that act at opioid receptors. These receptors are scattered throughout the body though mainly in the central and peripheral nervous system. Opiates are either derived from the opium poppy (morphine and codeine) or synthesised in the laboratory (pethidine). Opioids are indicated for pain at steps two and three of the WHO ladder (Table 20.5). This includes pain in patients with advanced disease and their short-term use to relieve breakthrough or severe acute pain of any origin.

The use of opioids for non-malignant chronic pain is controversial. In general, opioids on their own should be avoided for intractable chronic neurological pain (usually neuropathic) to reduce the risk of dependence. However their use in advanced or terminal disease should not be restricted as they are necessary and there is no risk of dependence in this setting. The biggest barriers to their use are availability and the stigma from both the doctor and the patient surrounding their use. Once these can be overcome they provide excellent pain relief. Whenever opioids are used, they should be given at regular intervals, e.g. morphine every 4 hours (oxycodone can be given 6 hourly), preferably via the oral route or when necessary via the parenteral route. The dose and frequency should be according to the needs of the patient and be reduced in renal or hepatic failure and in the elderly. Constipation is usually not a major issue in clinical practice.

It is important to realise that opioids are controlled drugs with strict regulations concerning their availability, prescription and use anywhere in the world. A major limitation to their use in many low income countries are the stringent national control policies regarding the accessibility and use of opioids for pain. However some countries in Africa have recently prioritized their use in pain control and opioids are available for medical use.

Adjuvants

These mainly include the antidepressants amitriptyline and the anticonvulsants carbamazepine and gabapentin or pregabalin. These are used in all three steps in the WHO analgesic ladder for the management of neuropathic pain. They are most commonly used as adjuvants in combination with opioids or non opioids depending on the severity of the pain. In some patients with chronic pain of neuropathic origin they are used on their own without analgesics. Examples of neurological disorders benefitting from their use include neuropathies (HIV & DM) and post herpetic and trigeminal neuralgias.

Their dose, route, frequency and side effects are outlined in Table 20.4. The main limitations are their side effects and frequency of administration which may limit patient compliance. It is always wise to start at the lowest dose and increase it slowly. In general antidepressants are taken once daily, often at night whereas anticonvulsants are prescribed twice or three times daily. The main side effects of tricyclics are anticholinergic and include sedation, dry mouth, postural hypotension and constipation among others. Side effects of the anticonvulsants include drowsiness (which often clears with regular usage), confusion and ataxia. Both antidepressants and anticonvulsants may be used together as they have different mechanisms of action in the nervous system.

Key points

Related posts:

COMA AND TRANSIENT LOSS OF CONSCIOUSNESS MYOPATHIES AND MYASTHENIA GRAVIS PARAPLEGIA NON TRAUMATIC HEAD AND SPINAL INJURY NEUROLOGICAL ILLNESS IN HIV DISEASE DISORDERS OF PERIPHERAL NERVES

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