Chapter 8. Neurological and psychiatric
Headache 218
Fits and faints 220
Stroke 223
Focal neurology 226
Falls and immobility 231
Delirium and alcohol withdrawal 233
Acute psychosis 235
Self-injury and self-poisoning 237
THE UNCONSCIOUS PATIENT
Consciousness and coma, respectively, may be defined as ‘a state of awareness of self and the environment’ and the absence of such awareness. Consciousness is dependent on the proper functioning of the ascending reticular activating system, a complex functional grouping of structures in the brainstem, thalamic and sub-thalamic regions.
Terms such as ‘drowsy’ and ‘obtunded’ are often used clinically, but are imprecise and liable to variable interpretations. Instead, the Glasgow Coma Scale (GCS) should be used to describe the level of consciousness (see ‘Acute scores’, p. 9). The scale is also valuable when monitoring the clinical course of an unconscious patient.
Coma and coma-like states
Classification of coma
The appearance of coma can be categorized, on clinical grounds, into three distinct groups. This classification is useful, as it can be used to determine the likely underlying pathology:
• coma with focal signs: stroke; intracranial tumour
• coma without focal signs but with meningism: subarachnoid haemorrhage; meningoencephalitis
• coma without focal signs or meningism: anoxic–ischaemic brain damage; metabolic, toxic or drug induced; meningitis; post-ictal.
Non-coma but coma-like appearance
In these states, the patient may be aware of their surroundings but, when examined, they appear to be in a coma.
Akinetic mutism
Classically seen in those patients who have suffered diencephalic damage, e.g. frontal tumours; encephalitis; end-stage CJD. These patients are immobile (akinetic), do not vocalize (mutism) and may not open their eyes.
Locked-in syndrome
This is a condition of tetraplegia and facial paralysis, with sparing of voluntary eye opening and vertical eye movements. It is usually caused by a pontine stroke.
Catatonia
This state is usually associated with psychiatric disease, but may also be seen with metabolic causes or with drug toxicity. The eyes are usually open with significantly reduced blinking. Passive limb movements may be associated with ‘waxy flexibility’.
Assessment
The assessment of any comatose patient should begin with ABCDE (see ‘Assessment of the acutely ill patient’, p. 8). Thereafter, take a history, asking the family or other contacts, as necessary, for information regarding recent events, past medical and drug history. A detailed neurological examination is essential. However, this should always be preceded by a general physical examination; specifically, look for rash, cyanosis, jaundice, fetor hepaticus and signs of chronic liver disease.
Neurological examination
Additional guidance is given on, p. 5.
Pupillary responses
A strong light source should be used. The pupillary responses are normal in toxic and metabolic coma. Opiates and atropine are among certain medications that will interfere with the physiological response.
Eye movements
Abnormal reflex eye movements (the oculocephalic or doll’s eye reflex) strongly suggest brainstem disease. Roving eye movements suggest a toxic/metabolic cause for the coma. Eye deviation, conjugate or dysconjugate, can also be useful in localizing the site of the structural lesion in coma.
Motor examination
Examination of the motor system is an essential part of the assessment in a patient with coma. Decerebrate rigidity refers to bilateral upper and lower limb extensor posture, usually the result of bilateral brainstem lesions. Decorticate posture refers to bilateral flexion of the upper limbs with extension of the lower limbs, usually suggesting an upper brainstem lesion. Asymmetry of signs can be very helpful as it suggests a structural cause of coma rather than a toxic or metabolic cause. Myoclonic jerks may occur in anoxic–ischaemic encephalopathies.
Investigations and management
Investigations
Initial investigations should focus on determining the underlying aetiology. These include BM and lab glucose, toxicology screen, liver function, CT brain ± EEG and LP. Potential complications should then be evaluated, e.g. aspiration (CXR) and intracranial pressure-induced bradycardia (ECG ± cardiac monitoring).
Management
The patient’s safety, the cause of their unconscious state (as above) and their longer-term support should all be considered.
When patients become unconscious suddenly, pay particular attention to their ability to protect their airway. Where their GCS drops below 8, they are likely to need airway support and ICU referral may be appropriate.
Where the period of unconsciousness is prolonged, nutrition and hydration will need to be considered. Initially, hydration can be maintained using intravenous fluids. Nutritional support should be instituted early and can be provided using a NG tube. Where long-term enteral feeding is required, insertion of a PEG tube may be more appropriate (see also ‘Nutrition’, p. 183)
When prescribing medication, consider the route that is most appropriate. Medications can be given IV where intravenous access has been obtained. If a NG or PEG tube is in situ, medication may be delivered by this route (check with a pharmacist or the BNF first).
Patients who are unconscious for any length of time are at increased risk of pressure sores and should be nursed appropriately; they should be turned regularly and their skin examined for early signs of pressure damage. They are also at risk of limb contractures and a physiotherapist should be involved early.
HEADACHE
Headache is a symptom that can have many causes. It can occur in isolation, as part of a primary headache syndrome, (e.g. migraine), or as a component of an evolving symptom complex suggestive of a secondary headache (e.g. brain tumour or meningitis).
Assessment
Initial assessment should aim to identify patients with clinical features suggestive of a secondary cause (see ‘Secondary causes of headache’, overleaf). In these patients, cranial imaging and further investigation should be considered.
History
Enquire about the following:
• onset and duration
• location, severity and quality of the pain
• frequency and timing of episodes
• associated features, aggravating and relieving factors
• past headache history.
Examination
In addition to a standard examination, the following features should be examined and documented:
• skin: for evidence of rash
• temporal artery: for tenderness and pulsation
• eye examination: including extraocular movements, pupils and fundi
• muscle power
• deep tendon reflexes and plantars
• coordination tests and gait.
Causes, investigation and management
Primary causes of headache
Tension-type headache
Bi-temporal and/or occipital headache of gradual onset. Can be due to stress-related neck and scalp muscle tension. Relaxation and simple analgesics should be used.
Migraine
Recurrent headaches which are throbbing in nature, associated with nausea, vomiting, light or sound sensitivity and which get worse with physical exertion are likely to be migraine headaches. Focal neurological symptoms, particularly visual symptoms, are characteristic.
The treatment of migraine involves consideration and avoidance of precipitants, e.g. caffeine, fasting, alcohol, cheese, chocolate. Stress and cyclical hormonal levels are also factors. Pharmacological management involves simple analgesics, such as aspirin or paracetamol, often in a combination preparation with an antiemetic, such as metoclopramide. Moderate to severe attacks of migraine can be treated with a triptan, such as sumatriptan given orally (50–100 mg), as a nasal spray (10 mg) or, if necessary, as a subcutaneous injection (6 mg). In recurrent migraine, β-blockers can be used for prophylaxis, e.g. propranolol 80–160 mg daily.
Cluster headaches
Patients suffering from cluster headaches are more likely to be male and give a history of short-lasting nocturnal headaches. These occur in a cyclical manner, are often retro-orbital and associated with redness and watering of the ipsilateral eye and restlessness. The attacks can occur repeatedly over several weeks.
Acute attacks can be alleviated by inhalation of high oxygen flow for 15 min ± sumatriptan 6 mg SC (for further dosing and cautionary notes, see the BNF). Verapamil can be used as a preventive agent (80–120 mg orally three times daily).
Secondary causes of headache
Cranial imaging ± further tests should be considered in patients with secondary causes of headache. These may present with the following clinical syndromes.
Thunderclap headache
A sudden-onset headache that reaches its peak within 1 min is termed a thunderclap headache. A ‘first or the worst’ headache should always be investigated. Important causes include:
• subarachnoid haemorrhage
• meningo-encephalitis
• internal carotid artery dissection
• cerebral venous sinus thrombosis
• acute hypertension
• pituitary apoplexy
• acute glaucoma
• benign orgasmic headache.
Subarachnoid haemorrhage
This typically presents as a thunderclap occipital headache, often described as ‘a massive blow to the back of the head’. Nausea and vomiting is commonly associated and signs of meningeal irritation, for example neck stiffness and Kernig’s sign, or an alteration in consciousness may be present.
If subarachnoid haemorrhage is suspected, a non-contrast CT scan of the brain should be performed immediately. If this test is normal, a lumbar puncture should be performed at least 12 h after the onset of the headache to look for xanthochromia (see ‘Lumbar puncture’, p. 37 and ‘CSF’, p. 74).
Management may involve surgical intervention or be conservative, including the use of nimodipine to reduce vasospasm in cerebral arteries. Urgent neurosurgical referral is advised in all patients.
Headache associated with raised intracranial pressure
Raised intracranial pressure (ICP) is suggested by a headache that occurs predominantly in the morning and gets worse with physical exertion, coughing and bending, or is associated with nausea and vomiting. Causes include brain tumours and idiopathic intracranial hypertension.
Signs associated with raised ICP include altered consciousness, papilloedema, III and VI nerve palsy. Hypotension and bradycardia suggest coning. Treatment should be directed towards the cause.
Headaches associated with CSF hypovolaemia
These typically get worse within 30 min of sitting up and get better promptly on lying down. CSF hypovolaemia is most commonly seen after a lumbar puncture, but can also occur spontaneously.
Medication overuse headaches
It is well recognized that overuse of any medication used for the acute treatment of headache can itself cause a rebound headache. This is true not only of opioid- containing analgesics, but also for over-the-counter analgesics and triptans. The only definitive treatment is withdrawal from the offending medication.
Others
If clinical features suggestive of any of the following diagnoses are present, appropriate investigation should be considered:
• head injury (with or without a haematoma)
• vascular event
• infection, including meningo-encephalitis and brain abscess
• vasculitis, e.g. temporal arteritis
• hypertensive encephalopathy
• trigeminal neuralgia.
FITS AND FAINTS
Seizures are short-lived, usually stereotyped events, caused by a burst or several bursts of electrical activity from the central nervous system. Awareness may or may not be impaired. Epilepsy (a tendency to have recurrent seizures) is a common neurological disorder with a prevalence of about 1 in 200. The social and medical consequences of a diagnosis of epilepsy mandate accurate and prompt diagnosis, appropriate classification and treatment.
Emergency assessment and management of seizures
Clinical assessment
It is often not possible to elicit a history from the patient since they will be either actively fitting or post-ictal. Ask any witnesses or family members for information regarding recent events, past medical and drug history. Enquire specifically about any prior history of fits, alcohol or drug ingestion. Common seizure presentations include:
• generalized tonic–clonic seizures: these are the most common seizure type noted in adults and consist of a tonic phase (stiffness, cry out and cyanosis), followed by a clonic phase consisting of alternating movements reducing in frequency and amplitude over several minutes, with subsequent confusion and drowsiness
• partial seizures: these result from an epileptic discharge that is restricted in distribution and can be subdivided into simple partial (with no alteration in awareness) or complex partial, where awareness of the environment is impaired and the patient has no recall of their activities.
More detailed clinical assessment is often not possible at this stage and emergency management should be initiated while simple investigations are performed; see below.
Investigation
Check BM and take bloods for FBC, U&E, LFT, Ca 2+, Glu and, if appropriate, blood cultures. If there is a concern about compliance with treatment, serum levels of any current antiepileptics should be measured.
Management
General measures
• assess ABC
• place in the recovery position and, if necessary, insert a nasopharyngeal airway
• if the patient has been fitting for >5 min, call for senior assistance
• give high flow oxygen and obtain venous access
• if BM is <3.5 mmol/L give 100 mL of 20% dextrose IV
• monitor pulse, BP, temperature and heart rhythm.
Control of seizures
Local protocols may be available and should be consulted. In general, benzodiazepines should be used first-line:
• lorazepam 2 mg IV over 4 min, repeated if necessary after 10 min, or
• diazepam 10 mg PR if no IV access
• if the patient is malnourished or alcoholic, give Pabrinex®, two pairs of vials IV over 10 min.
If one dose of benzodiazepine does not control the seizures (remember that this may have been given already by paramedical staff), then senior assistance should be called and IV phenytoin should be administered (15 mg/kg at 50 mg/min unless already taking oral phenytoin). In some hospitals, intravenous valproate can be used either first-line, or where the patient is on phenytoin. If these strategies fail to control the seizures, then the patient will most likely have been fitting for >30 min and has status epilepticus.
Status epilepticus
Status epilepticus is defined as a seizure lasting >30 min, or successive seizures with no recovery of awareness in between. It can arise either as a complication of recognized epilepsy (brought about by poor compliance, alcohol use, or illicit drug use) or as an initial presentation of epilepsy (secondary to encephalitis, trauma, drug use, or alcohol withdrawal). Status epilepticus is a medical emergency with a mortality of around 30%. Adequate diagnosis of any primary cause and appropriate treatment is vital in speeding recovery and minimizing complications.
Clinical features, investigation and treatment
Remember that while clonic movements may predominate in the early stages, these will become less pronounced with time. Recovery from status should not be assumed because movement has stopped. Where impairment of consciousness continues, an EEG should be performed to confirm that the ictal activity has stopped.
Whether there is pre-existing epilepsy or not, patients with status should have cranial imaging and, if there is a suspicion of encephalitis, a lumbar puncture. All patients should be referred to ICU and considered for ventilation and administration of a general anaesthetic to control seizures.
Elective assessment of a possible first fit
This is a frequent presentation to medical clinics, GP surgeries, and A&E departments. Do not assume that the cause is epilepsy, since approximately 50% of patients referred to a ‘first seizure’ clinic will have another explanation which becomes apparent with time.
Clinical assessment
The most important step is to differentiate seizure from syncope (Table 8.1). ‘False positive’ clinical diagnoses of seizure can result from a description of short-lived jerking movements that are not uncommon with syncope.
| Syncope | Seizure | |
|---|---|---|
| Prodrome | Precipitants are common | Unprovoked |
| Hypotensive | Occasionally focal positive neurological symptoms | |
| Visual disturbance | ||
| Nausea | ||
| Palpitations | ||
| Hyperventilation | ||
| Ringing in ears | ||
| Eye witness account | Pallor, sweating | Cyanosis |
| Short-lived (<1 min) | Jerking limb movements of reducing frequency and severity | |
| Intermittent jerking of limbs | ||
| Recovery | Rapid recovery (<5 min) | Sleepy afterwards |
| Brief disorientation (seconds) | Confused | |
| Urinary incontinence | Urinary incontinence | |
| Tongue bitten (tip) | Tongue bitten (sides) | |
| ‘Washed out’ | Dysphasia or other negative neurological symptoms |
Specific enquiry should be made about general health (especially cardiac, diabetic, renal or hepatic disease), previous ‘fits’ in adult life or childhood, possible pregnancy, alcohol intake or recreational drugs (including the timing of last intake) and a family history of epilepsy or seizure.
When taking a history from a patient who has previously lost consciousness, it is important to ask about other potential seizure events, e.g. nocturnal episodes, myoclonic jerks, partial versus generalized seizures (see above). This information can help with the diagnosis and classification of any epilepsy.
Investigation
All patients should have an ECG carried out following an episode of blackout. Patients who have had a definite single seizure should have cranial imaging (CT, or ideally MRI) to exclude an intracranial lesion. An EEG will not help differentiate seizure from syncope, but may help in giving the patient advice about prognosis.
Treatment
In the UK, patients presenting with a possible first seizure, who have no risk factors for the development of epilepsy, are not routinely prescribed anticonvulsants. Patients without neurological deficit do not need admission provided they have someone at home to look after them. However, all patients with suspected first seizure should be given advice regarding driving eligibility (see ‘Driving’, p. 411).
Management of established epilepsy
Treatment
Long-term treatment for epilepsy should not be started by non-specialists. The dangers of inappropriate treatment, lists of pharmacokinetic interactions and recommendations for optimal dosage and combinations are complex and best considered in conjunction with national guidelines (SIGN 70 and NICE). Admission and driving concerns should be addressed as described above.
STROKE
A stroke may result from embolism from a distant site (usually cardiac), arterial thrombosis or haemorrhage into the brain substance. Stroke is the third most common cause of death in developed countries and is one of the most important causes of severe disability.
Recent advances in neuroimaging techniques have increased our understanding of cerebrovascular disease and enabled decisions regarding treatment to be made early. The development of stroke units has been another important step in ensuring provision of the best available care. Nevertheless, clinical history and examination remain the most important tools in the assessment of patients with stroke.
Diagnosis
Presentation
The sudden onset of focal neurological symptoms is the hallmark of a vascular event such as a transient ischaemic attack (TIA) or stroke. Therefore, it is useful to ask patients what they were doing at the time. At least half of all TIAs or strokes occur in the morning and patients often wake with a neurological deficit. Table 8.2 lists focal neurological symptoms that may suggest a TIA or a stroke.
| Type of injury | Symptoms |
|---|---|
| Motor | Weakness or clumsiness of one side of body (mono/hemiparesis) |
| Bilateral weakness | |
| Swallowing problems | |
| Unsteadiness | |
| Sensory | Altered feeling on one side of the body (para/quadriparesis) |
| Speech and language | Difficulty in understanding or expressing speech (dysphasia) |
| Reading difficulties (dyslexia) | |
| Writing difficulties (dysgraphia) | |
| Slurred speech (dysarthria) | |
| Visual | Loss of vision in one eye |
| Visual field defect: hemi or quadrantanopia | |
| Double vision | |
| Others | Vertigo |
| Amnesia | |
| Visuospatial symptoms |
The duration of symptoms is of paramount importance in differentiating stroke from other neurological conditions (Table 8.3, overleaf). A TIA is classically defined as a focal neurological deficit lasting <24 h and a stroke as a deficit lasting >24 h. However, neuroimaging techniques have blurred this distinction. Moreover, the advent of thrombolysis for some patients may require a revision of these criteria.
| Timing | Pathology | Associated features |
|---|---|---|
| Abrupt onset | Vascular: | |
| Infarction | Risk factors | |
| Haemorrhage | Pain, space occupying effects | |
| Variable or fluctuating course (days to weeks) | Demyelinating | Previous minor neurological symptoms |
| Temperature sensitivity | ||
| L’hermitte’s sign | ||
| Progressive (days to weeks) | Neoplastic | Focal neurological symptoms or features of raised ICP |
| Systemic features of neoplasm | ||
| Degenerative | Onset in late or middle age | |
| Static or progressive from early life | Congenital or genetic | Positive family history |
The diagnosis of stroke is usually straightforward, as the patient has a persisting neurological deficit at the time of presentation. A TIA, however, can pose considerable diagnostic difficulty because, in many patients, the symptoms resolve completely within 1 h. Migraine and epilepsy can be mistaken for a TIA and a careful history is essential.
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