Back pain is a huge problem for many patients world-wide. The incidence in the general population is 5% and the lifetime prevalence is 60-90%. Most of these patients have chronic or relapsing symptoms and most will not have a specific diagnosis made.
The causes of back pain are many: the main issue when seeing a patient with back pain is to differentiate between ‘organic’ and ‘non-organic’ causes and to identify any ‘red-flag’ symptoms/signs:
Age <20 or >70
PMHx of neoplasia or osteoporosis
Unexplained weight loss
Constant pain that’s worse at night
Acute onset of incontinence (fecal or urinary) or urinary retention
Loss of perineal sensation
Global and progressive weakness of the lower limbs
Mechanical back pain; prolapsed disc; spondylolisthesis; Fracture; Ankylosing Spondylitis; Infection
1st line treatment remains advice and reassurance: minimal bed rest; low stress aerobic exercise and minimal disruption to activities of daily living (ADL). Most cases of mechanical back pain will resolve within 1 month. If pain is impeding ADLs, persists for longer than one month (assuming it is not worse and more serious pathology has been excluded) or the patient is relapsing frequently, simple regular analgesia (paracetamol +/- NSAIDs) is usually effective. Altering the strength of analgesia should be done following the analgesic ladder.
Surgery should only be considered 3rd line in patients who are fit and able. Much of the surgery done for back pain is not highly successful.
Wash hands, introduce self, check patient name and DOB, establish rapport and gain consent
e.g. acute onset associated with heavy lifting (mechanical)
acute onset after coughing/sneezing or twisting or after earlier strain (prolapsed disc/spondylolisthesis)
gradual onset (stenosis/tumour)
Radiation/associated sensory features
Buttocks/back of leg- sciatica (prolapsed disc/spondylolisthesis)
Saddle anaesthesia- Red flag for cauda equina (anterior prolapse)
Foot/inner thigh numbness
e.g. walking uphill (stenosis)
Incontinence- another red flag for cauda equina
NB paralysis is another red flag
You also want details in the rest of the history e.g. FHx back problems, Employment involving heavy lifting; previous back injury/trauma/conditions/surgery etc;
Wash hands, Introduce, Check name of date of birth, opening question
If a single fall (or regarding the worst fall):
Has there been loss of consciousness, injury etc and if so, how long were they fallen? Who found/finds them?
Is there anything that precipitates a fall (any dizziness, any movement, any breathlessness, any funny feelings)? Do they occur when taking your medication? Do they occur in dark places? Is it on the stairs? (Think of DAME)
Drugs (& toxins e.g. alcohol/medications); Age-related factors (sarcopenia, immobility); Medical conditions; Environment
After a fall do you feel ok? How long?
Re: more than one
How many? How often?
Have they been getting worse with time (more/less frequent)?
Medical and drug history are very important?
Heart conditions- BP drugs? Anti-arrhythmics? Anti-coagulants?
Epilepsy and drugs?
Social History is also very important
Living situation: on their own- self-care / home-help / family; living with someone else; house environment- stairs/rails; clutter etc
Do they get out of the house? Can they do daily tasks e.g. shopping; cooking; cleaning? How do they get about? (stick/zimmer/chair/rail etc)
NB Family Hx not so important
Conditions for admission
cannot walk; acute illness or if they are falling so frequently that home would be unmanageable/too great a risk.
Examine standing still, checking balance. Do Romberg’s test: ask the patient to close their eyes and see if sway worsens (in cerebellar disease, patients can sway to the ipsilateral side). Also do Trendelenburg’s test– ask the patient (with eyes open and with your support) to stand on one leg for 30s (In weakness/structural/pain problems of the hip adductors, the contralateral hemipelvis will drop)
Watch the patient walk a few metres, turn and come back again. Look from all angles.
Trendelenburg gait (trunchal lurch to the affected side); spastic gait (hyperextented leg); Parkinsonian gait (shuffling; slow to start; no arm swing); cerebellar ataxia (broad-based gait)
Do they need support?
Examination of limbs
On the bed, inspect the limbs for lengthening/external rotation (hip fracture). Also look for any other signs.
Feel the hip and knee joints for deformity/tenderness.
(On the bed, carry out Thomas’s Test: Flex both hips and knees and place your hand under the lumbar spine. Ask the patient to extend the testing hip (A fixed flexion deformity will make this difficult).)
NB In practice, many (particularly elderly) patients, will have difficulty doing this. Furthermore, as it rarely will change the management of a patient, it is no longer routinely performed, although it may still be taught and required in an OSCE
Test range of movement (passive and active) of the hip and knee and foot
Underlying causes and complications of falls are numerous, but the following associations warrant more immediate evaluation:
Any history of or current change in alertness or level of consciousness: possible causes include cerebrovascular (transient ischemic attack, stroke, seizure), cardiovascular (hypotension, bradycardia or tachycardia), or infectious causes. 
Head trauma: anticoagulation or antiplatelet therapy raise concern for a subdural hematoma. 
Pain suggesting a potential fracture: persistent pain, inability to bear weight, or any obvious anatomical abnormality should prompt a quick evaluation for fracture, along with appropriate orthopedic consultation. Consideration should be given to treating osteoporosis in patients with fractures relating to low-impact falls. 
Visual impairment: may manifest as blurred vision or diplopia.
Peripheral neuropathy: may be accompanied by a history of diabetes or neurodegenerative disease.
Vestibular dysfunction, particularly benign paroxysmal positional vertigo: may manifest itself as dizziness, vertigo, or imbalance.
Gait and balance disturbance: possible history of disc disease, peripheral neuropathy, arthritis or prior injury; specific abnormality may suggest underlying disorder such as Parkinson disease.
Fear of falling itself can be a factor in increasing the risk of falls.
Cognitive or mood impairment: includes dementia, depression, or delirium; behavioral disturbances, functional impairments, and the use of neuroleptics may all contribute to falls.
Seizure disorder: may have vascular, infectious or malignant causes.
Subdural hematoma: suggested by head trauma in the presence of anticoagulation.
Cerebrovascular accident or transient ischemic attack: focal neurologic symptoms of nontransient or transient duration, respectively.
Syncope: for example, cardiac syncope caused by tachyarrhythmias or bradycardia, or vasovagal syncope caused by an abnormal or exaggerated autonomic response to stimuli such as standing or emotion.
Orthostatic hypotension: suggested by positional symptoms.
Carotid sinus syndrome: may be elicited by activities such as facial shaving.
Postprandial hypotension: event documented based on history of observed fall coincident with meal times.
Joint buckling/instability: may be due to prior injury.
Mechanical mobility/gait abnormality: patient may have prior fracture or arthritis.
Deconditioning: insufficient exercise is common with aging.
Medications: especially benzodiazepines, antidepressants, and antipsychotics; others associated with an increased risk of orthostatic hypotension include alpha-blockers, antipsychotics, antihypertensives, diuretics, beta-blockers, bromocryptine, levodopa, nonsteroidal anti-inflammatory drugs, marijuana, narcotics and sedatives, hypnotics, sildenafil, tricyclic antidepressants, and vasodilators; there is some suggestion that high-dose cholecalciferol supplementation (500,000 IU once yearly) is associated with an increased risk of fall and fracture.
Polypharmacy; use of 5 or more medications increases the risk of falls by 30% in community-dwelling people, and by at least a factor of 4 in nursing-home patients.
Substance abuse: including alcohol (chronic misuse or acute intoxication) or OTC medications.
Environmental hazards such as loose rugs or tiles, poor lighting, recent use of a cane or walker, or living alone: these factors are of increased importance with age.
Inflammation of the tonsils secondary to infection. NB Pharyngitis is inflammation of the oropharynx without tonsillar involvement.
Most cases of ‘sore throat’ will be viral and will be self-limiting, non-serious disease. However, and in children especially, 30% of cases are bacterial
Almost entirely Group A β-haemolytic Strep (Strep pyogenes) (other causal organisms include S aureus, S pneumoniae, M pneumoniae, Moraxella catarrhalis, H influenzae etc)
Sore throat, may refer to the ears
Red, swollen throat and tonsils
The patient may have noticed foul smelling breath
There may be a yellow-white exudate covering the tonsils
There may be changes in voice and dysphagia may be a problem
There may be associated lymphadenopathy of the neck.
Abdominal pain, headache and fever may also be present.
Centor criteria for diagnosis (3 or 4 present merits antibiotic treatment)
tender anterior cervical lymph nodes
history of fever
absence of cough
Not usually necessary (unless it will alter treatment e.g. if the condition doesn’t respond to treatment)
I.e. Do NOT take throat swabs- these can often be misleading. Many people are carriers for Group A Strep and others will not grow anything on culture but have clear clinical evidence of infection.
Paul Bunnell test is usually indicated (mononucleosis/EBV- glandular fever)
According to the antibiotic man (Tayside area formulary- primary care), penicillin V (oral 1g BD or 500mg QDS for 5 days in adults; 10 days in children (dose calculated by weight in kids too) can be given to patients who fulfill 3 or more of the Centor criteria
But they add that this will only shorten the duration of illness by 1/7 days (on average)
Centor criteria (3/4 suggest GABHS tonsillitis- may benefit from antibiotics)
Presence of tonsillar exudate
Presence of tendor anterior cervical lymphadenopathy
History of fever
Absence of cough
Or in those with marked systemic upset; unilateral peritonsillitis; a history of rheumatic fever; an increased risk from acute infection (such as a child with diabetes mellitus or immunodeficiency)
Alternatively, clarithromycin can be considered (500mg BD for 5 days)
However, antibiotics should be used sparingly (not really for symptomatic relief)
DO NOT prescribe penicillin (particularly amoxicillin) in suspected cases of (or without ruling out) EBV as this could precipitate a maculopapular rash
Ibuprofen (400mg TDS) and/or paracetamol can be used for symptom relief
SIGN recommends that surgery (tonsillectomy) be considered for patients with recurrent acute sore throats lasting at least a year
due to tonsillitis
seven or more significant and adequately treated sore throats in the preceding year OR 5 or more in the each of the last 2 years (10) OR 3 or more in the each of the last 3 years (9)
NICE suggests 5 in the last year
NB Surgery should be avoided, where possible, in children with sore throat. Watchful waiting is more appropriate
NSAIDs, antiemetics (postoperatively) and a single dose of dexamethasone (at induction of anaesthetic) can be used for peri/postoperative managements of pain and nausea/vomiting (respectively)
Elevate head >30° off bed (increases venous return and decreases ICP)
Monitor neurological status closely; assess for pain/restlessness regularly
Administer analgesia as required (AVOID narcotics)
Manage in a dark, quiet room
Assess response to treatment regularly
IV Ceftriaxone2g BD
+ IV Ampicillin/Amoxicillin 2g QDS if listeria is suspected (and in >55yo)
IV amphotericin B/ flucytosine / fluconazole if cryptococcus suspected (HIV)
Rifampicin, Isoniazid, Pyridostigmine and Ethambutol for TB
If Penicillin Allergic
Chloramphenicol IV 25mg/kg and Vancomycin IV 500mg QDS
+ Co-trimoxazole if suspect listeria
Empiric treatment (child)
Ceftriaxone + amoxicillin (basically as long as there is a 3rd gen cephalosporin: ceftriaxone/cefotaxime (2nd gen: cefuroxime can be used too- more useful for resistant infections) to cover Niesseria/E coli and a penicillin to cover strep, I think you’re covered. Gentamicin will help the action of penicillins and will provide some coverage against gram negatives BUT it has ototoxic/nephrotoxic risk so a risk/benefit decision should be made there and then. In general, I don’t think it is first line, but as soon as cultures come back, should be added if appropriate)
If group B strep: benzylpenicillin and gentamicin
If listeria: amoxicillin and gentamicin
If paracetamol hypersensitive: as adult
Give to all patients suspected of bacterial meningitis:
10mg IV 15-20mins BEFORE or with the first dose of antibiotic, then every 6 hours
Contraindicated in post-surgical meningitis; severely immunocomprimised; meningococcal/septic shock or hypersensitivity
Worse if showing organ failure/distress or increasing sepsis
Spinal cord tumours e.g. gliomas; ependymoma or metastases
Onset is usually gradual (weeks) but can be acute e.g. in traumatic, metastatic or vascular causes
Localised over the spine (this is a common early symptom, particularly in patients with metastatic disease- i.e. DO NOT ignore this in these patients) and/or in a radicular distribution (may be aggravated by coughing, sneezing, straining)
Paraesthesia and numbness which often begins in the lower limbs and spreads up, often to a specific level on the trunk
Can be loss of proprioception, light touch or pin-prick sensation
Can also cause a reduction in proprioception depending on extent of compression (often later than light sensation; particularly in anterior compression syndromes where the dorsal columns are the last to be affected)
Motor (late but common)
Weakness or stiffness of the limbs (lower > upper)
Weakness may be hard to determine if the patient is not walking prior to symptom onset
Can be bilateral or unilateral
Urgency or hesitancy of micturition, progressing to urinary retention
Typically, there are a mixture of upper and lower motor neuron signs
Below the level of compression there are usually upper motor neuron signs i.e. brisk reflexes and spasticity
At the level of compression there are usually lower motor neuron signs (due to compression of the nerve roots as well as spinal cord) i.e. hyporeflexia and weakness
Above the level of compression, signs can be normal
Signs of injury at different spinal levels
Cervical (above C5)
Upper motor neuron signs in all limbs and diaphragmatic weakness (phrenic nerve affected)
Cervical (at or below C5)
Lower motor neuron signs and segmental sensory loss in the arms; upper motor neuron signs in the legs
Respiratory (intercostal) weakness
Spastic paraplegia with a sensory level at the trunk
Weakness of the legs, sacral loss of sensation and extensor (upward) plantar reflexes
Specific syndromes associated with cord compression (often traumatic/hyperacute causes)
Cord transection i.e. complete lesion (all motor and sensory modalities affected)
Complete loss of motor control and sensation from the anywhere below the level affected
Initially a flaccid arreflexic paralysis (spinal shock) with hypotension, bradycardia and hypothermia (classic triad)
UMN signs later on
Unlikely to recover
Brown-Sequard Syndrome (Cord hemisection- very rare but produces some classical signs to note; NB can be due to compressive lesions so may present slowly)
Disruption of the ipsilateral motor pathways; ipsilateral dorsal column tracts (fine touch/proprioception/reflexes) and contralateral spinothalamic tract
Central cord syndrome
usually caused by a hyperflexion/hyperextension injury to an already stenotic neck
Predominantly distal upper limb weakness; cape-like spinothalamic sensory loss (lower limb power and dorsal column sensation preserved)
Arrange an URGENT MRI (as soon as possible)
Depends on cause
ABCDE; Immobilise; investigate (X-ray/MRI)
Methylprednisolone(Must be given within 8 hours)- Bolus and 24hr infusion
Decompress and stabilise
Depends on tumour/patient
Dexamethasoneas soon as possible
16mg IV stat then 4mg PO QDS + PPI cover
Reduces vasogenic oedema
Radiotherapy or Surgery if clinically suitable
Surgery if single level involvement without widespread disease; or radio-resistant disease/previous radiotherapy to the site OR if unknown primary
Chemotherapy can only really be considered in rarer highly sensitive tumours
Antimicrobial treatment- (High dose IV Ceftriaxone and Metronidazole +/- Flucloxacillin if staph aureus involvement)
Reverse any anticoagulant and surgically decompress
Aura is a fully reversible visual, sensory, motor or language symptom that usually lasts 20-60 mins. Headache usually follows <1hr later but the two can occur simultaneously. Visual aura is the most common type. Positive monochromatic symptoms e.g. central scomata; central fortification; hemianopic loss
This is a clinical diagnosis
the patient must have had at least 5 attacks lasting a total of 4-72 hours
2 must have been moderate/severe, unilateral, throbbing pain, made worse with movement
1 must have had some autonomic component (normally photo/phonophobia)
Both vascular and neural influences cause migraines in susceptible individuals
Theory is that migraine is a primary neurogenic condition but secondary vascular changes cause worsening symptoms
Stress triggers changes in the brain, these changes cause release of serotonin (can be affected by sleep, diet, stress, hormones, exercise etc)
Blood vessels constrict and dilate
Chemicals including substance P irritate the nerves and blood vessels causing pain
Aura is caused by
Cortical spreading depolarisation (spread of excitation)
Activation of the trigeminal vascular system- dilation of cranial blood vessels
Release of substance P, neurokinin A and CGRP
Acephalgic (relatively rare: symptoms of migraine without headache i.e. aura, photophobia, nausea etc)
The trigeminal autonomic cephalgias are a group of primary headache disorders characterised by unilateral trigeminal distribution pain that occurs in association with prominent ipsilateral cranial autonomic features e.g.
Ptosis; miosis; Nasal stuffiness; Nausea/vomiting; Tearing; eye lid oedema
NB IMPORTANT: Anyone with new onset, unilateral cranial autonomic features requires imaging with MRIb/MRIangio to exclude vascular/mass causes that could have severe consequences
30-40 years old
Circadian and seasonal
Severe unilateral headache lasting 45-90 mins (20mins – 3hrs)
Occurring 1-8 times/day
Occur in ‘clusters’ that can last weeks/months
Acutely: high flow oxygen (100%) and subcut sumatriptan (6mg)
Short-term: Steroids (2 weeks- reducing dose)
Long-term: Verapamil (prophylaxis)
Women > Men
50-60 years old
Severe unilateral headache with pronounced unilateral autonomic features
Lasting 10-30mins (2-45mins)
Occurring 1-40 times/day
i.e. shorter duration but more frequent than cluster
Treat with indomethacin (patients usually have an absolute response)
Essentially the same as P/H but features are persistent
There is an equally good response to indomethacin
Short lasting Unilateral Neuralgiform headache with Conjunctival Tearing/injection- SUNCT
Male > Female
Short lived (15-20 sec), unilateral neuralgiform (i.e. nerve pain) headache
With conjunctival tearing or injection (dominant autonomic feature)
Treat with gabapentin
Trigeminal Neuralgia(technically not a TAC as there are rarely any autonomic features)
More common in the elderly
Pain is triggered by touch and usually occurs in a particular facial distribution (V2 or V3)
Pain is severe and stabbing; brief (1-90sec) but can occur 10-100 times/day
Bouts of pain may last weeks/months before any sort of remission
Treat with carbemazepine/gabapentin/phenytoin/baclofen
Surgery may also be used to ablate/decompress the affected nerve
MRI is only indicated if there are focal signs, atypical features, poor response to medication or prior to surgery
Make sure to differentiate between focal weakness, generalised weakness and lethargy/malaise (e.g. anaemia)
NB Local weakness (i.e. unilateral and of specific muscle groups) suggest a neuropathy of some description (this could be radiculopathy, but could also be due to a compressive lesion/trauma or even early on in ALS)
Ask about where the weakness is worst?
Proximally vs Distally vs everywhere (MG/polymyositis vs GB/myelopathy vs ?CFS)
How long has it been going on for?
Any time/exertions make it worse?
Exertion (better in LES; worse in MG/polymyositis)
End of day (MG) vs All the time (CFS) vs start of day (CFS)
Do they have trouble doing ADLs?
Washing etc etc
Are there any other symptoms?
In particular pain or loss of sensation?
Where- dermatomal/nerve root distribution / proximally / random non-specific
? Cancer syndrome; hypothyroidism; anaemia
Ask about problem of weakness elsewhere e.g. dysphagia, dysarthria, gait problems; and impact on daily life
The rest of the history is as expected i.e. systemic enquiry (important); PMHx; RHx/ FHx/ SHx etc. Be sure to ask about recent illness e.g. gastroenteritis (GBS); history of cancer (LES); drugs (STATINS); family history (DMD); social history, etc etc
In contrast to motor examination, begin distally and work proximally for sensation
Before testing a mode of sensation show the patient what you are going to do by testing it on the top of the sternum with their eyes open
Begin by using a cotton wool bud to test light touch (dorsal column). Ask the patient to close their eyes.
Touch the limbs with the cotton wool beginning at the tips of the fingers/toes and then working up
You then want to test the dermatome regions
Repeat with a neurotip pin, test pain (spinothalamic)
With a 128Hz tuning fork, test vibration sense on bony prominences, again beginning distally
Holding the joint at the sides and with the patient’s eyes initially open, demonstrate upward and downward movement of the distal finger (or other joint). Ask the patient to close their eyes and move the joint up or down and ask the patient to tell you which way you are moving it.
If the patient cannot do this, move proximally until they can.
Some indicative tests of Myaesthenia
Ask the patient to count to 100.
If the patient becomes dysarthric after a while, this points towards MG
Ask the patient to look at your finger and raise it up so they have to look up at it. Keep their gaze there for a minute or two.
Again, patients with MG lose the ability to hold gaze upwards and eyelids begin to droop.
Have a general look at the patient – do they look ‘flat’?
MSK examination of the limbs/neck/back may also be required.