The human body is just a system for keeping the visual system alive - Prof Dutton
Dyskinetic CP associated with poor focusing (as is Downs) – bifocals may be helpful.
Blindsight - the primitive visual system, that bypasses the cortex and therefore may persist even where damage to the visual cortex renders the person blind. When asked to respond to visual stimuli that they have no qualitative awareness of, they tend to do better than expected by chance. Tends to be peripheral, and is quickly fatiguable, so change sides often eg spoon feeding, .reduces feed times if alternate sides.
Enterovirus is the most common cause of aseptic meningitis in the UK, although in some locations in other parts of Europe there are specific local arboviruses (mosquito borne) that are more common. In adolescents, associated with severe headache. CSF classically shows lymphocytosis but actually may contain up to 1000 neutrophils. PCR for enterovirus is sensitive in the first 2 days of clinical symptoms but sensitivity falls off thereafter. Stool PCR on the other hand can remain positive for 5-16 days. Clin Infect Dis. 2005 Apr 1;40(7):982-7. Epub 2005
DXM reduces CSF pressure, pleocytosis, lactate and TNF! Causes more rapid defervescence - but not the same as better cure, and beware resistant bugs. Don't use in babies under 6 weeks (why?).
0.4 mg/kg BD for 2 days shown to be pharmacologically more rational, and safer than earlier 0.15 mg/kg QDS for 4 days.
Pediatric Infectious Disease Journal. 23(4):355-357, April 2004.
8% of the "complicated" (eg neonatal, convulsions, relapse) cases and 5% of "uncomplicated" meningitis cases attended a special school at age 13yr. More likely to be getting extra help at school, even if no or mild disability at 5 years.
See also TB under Infection. Often gradual onset and no meningism so beware history of odd behaviour, change in conscious level. Typical CSF findings are of high protein, lymphocytosis with low glucose. A Spider's web clot is characteristic, due to the gelatinous exudate associated with infection that in turn causes cranial nerve palsies and obstructive hydrocephalus. Vasculitis may cause focal neurological signs. CXR may be helpful if no AFBs seen; remember to get good family history!
A cerebral tuberculoma may give similar presentation but without CSF signs...
Can be primary HSV infection, reactivation or second infection! Untreated, herpes simplex encephalitis (HSE) is associated with a 70% mortality rate. With aciclovir, mortality is cut to 30%, although morbidity remains high. Predisposition for affecting the temporal and frontal lobes, leading to the classic clinical findings of aphasia, temporal lobe seizures, personality changes, and focal neurologic deficits. Altered mentation, hemiparesis, dysphagia, and ataxia are also common finding.
Diagnosis by imaging, EEG and lab tests.
Curr Op Peds 16(5); 2004.
Standard treatment is for 3/52, Scot treats for 10 days - but being PCR positive at the end of treatment is the only known prognostic marker, so continue until negativity achieved, however long that takes! Oral aciclovir is not effective for suppression in neonates and no data in older children.
PIDJ Volume 25(9), September 2006, pp 841-842
Strong geographical variation. Enterovirus common, but often no agent identified. But other possible causes are:
Differential includes Reyes syndrome. Clinical course unpredictable. Can be mild initially with sudden decompensation and death, else severe but relapsing with intermittent clarity (generally a good prognosis).
Diverse causes, some of which are extremely serious (mostly infiltrative):
Bell's Palsy is what you would call it if idiopathic, but perhaps you just haven't looked hard enough? Often otalgia, facial or retroauricular pain. Typically mild except in Zoster, where it is severe. Pain may precede palsy.
Warning signs (for a serious underlying cause) are:
Assess using House-Brackmann scale. Management: do hearing test, blood pressure, check frontal sparing/tongue/finger function. FBC if any suspicion of leukaemia. Check blink reflex (prognostic).
Treatment:
Recovery usually within 3 weeks, else nerve regeneration takes 4-6 months. Beyond 6 months improvement is unlikely. For long term palsy, feedback training, surgical techniques may result in functional as well as cosmetic improvements. Synkinesis and facial spasm are complications, treat with botulinum. (BMJ 329:553)
Consider inflammatory and non-inflammatory causes. Non inflammatory -
Inflammatory causes -
CurrOpPeds Dec 2004
Brain MRI is best, should be undertaken as soon as possible after presentation. If not available within 48 hours, CT is an acceptable initial alternative. Do urgently in children with depressed level of consciousness or who are clinically deteriorating. Assuming you have evidence of acute arterial ischaemia, continue as below.
Imaging of the cervical and proximal intracranial arterial vasculature should be done. Cervical imaging (to exclude dissection) should be done within 48 hours.
Echo should be done within 48 hours.
Investigate for prothrombotic tendency:
Aspirin (5mg/kg/day) should be given once there is radiological confirmation, except in patients with evidence of intracranial haemorrhage on imaging.
Anticoagulation should be considered (unless there is no haemorrhage) if
Early neurological referral should be considered if depressed or deteriorating conscious level or other signs of raised intracranial pressure.
Children with moyamoya syndrome should be referred for evaluation to a centre with expertise in evaluating patients for surgical revascularisation.
Advice should be offered regarding preventable risk factors for arterial disease in adult life, particularly smoking, exercise and diet. Blood pressure should be measured annually to screen for hypertension.
To prevent disability, as soon as possible after admission evaluate:
RCPCH Guideline August 2004 Stroke in Children
Causes:
Post-streptococcal dyskinesias (chorea , motor tics, dystonia, tremor, stereotypies, opsoclonus and myoclonus) occur with significant and disabling psychiatric co-morbidity (various and common) and are potential autoimmune models of common "idiopathic" movement and psychiatric disorders in children. Sex is important: most choreas are in girls, most tics in boys. PANDAS (paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) diagnosed when symptoms worsen with strep infections.
(ArchDisChild 2004;89)
In minor head injury (definition?!), statistically significant correlation between intracranial haemorrhage and:
Headache and vomiting were not found to be predictive and there was great variability in the predictive ability of seizures. (meta-analysis)(ArchDisChild 2004;89)
SIGN 110 suggests immediate CT for:
Otherwise, early (ie within 8 hours) CT should be considered if:
Also recommends CT "as soon as child is stable" (and ideally within 24 hrs) if suspicion of NAI and under 1 yr, or neuro signs (incl haemorrhagic retinopathy).
Any loss of consciousness should be assessed, but interestingly retrograde amnesia has to be for >30 minutes to warrant assessment! Otherwise 2+ vomits, severe and persistent headache, coagulopathy, difficulties with assessment or social situation, or any other indication for CT.
Admit if any indications for CT, although it also says discharge can be considered if social situation suitable!
NICE head injury (June 2003) very similar. Change in practice from admit and watch (Royal College of Surgeons guidelines) to diagnose and decide. Leads to far fewer skull XRs, a lot more CTs and maybe half as many admissions. Some centres have seen cost savings due to earlier discharge.
CT immediately for:
In children under 10yr, CT for spine should be avoided (risk to thyroid) unless severe head injury (eg GCS<=8), strong suspicion despite plain films, or inadequate plain films. Over 10yr, CT is investigation of choice if:
Neuroscience centres are expected to be able to perform initial management of multiple injuries in children. Local guidelines for transfer should be drawn up – there are benefits for being in a neurosurgical centre even if surgery is not required.
Kids with a fracture are not as prone to intracranial lesions as adults, at the same time they are more likely to have intracranial lesion without a fracture!
No good RCTs! Avoid secondary brain injury - 1 episode hypotension post head injury triples mortality. Cerebral blood flow is low in first 24hr, peaks at 48hr. Depends on temperature, seizures, pain/anxiety.
Glasgow Coma Score (GCS) 9-12 is moderate, <=8 is severe (equivalent to P or U in AVPU score) and is indication for ventilation to protect airway as reflexes potentially unreliable.
Diffuse axonal injury progresses over 24+ hrs, difficult to see on scan.
Consider external drain/ventriculostomy for intracranial haemorrhage. ?Remove contused brain ?Decompressive craniectomy
Neuroprotective strategy:
For RICP, 3% NaCl 3-5ml/kg bolus - Keep osmo <310mmol/l.
For induction, thiopentone is traditionally used. Ketamine theoretically increases ICP but no real evidence. Adding fentanyl smooths cardiovascular response to procedure.
CT@72h is prognostic.
Shaken Baby: lethargy, vomiting, apnoeas, seizures (40-80%), opisthotonus, irritability. See Social.
Melatonin secretion becomes regular cycle by 3 yrs. Babies have active sleep equivalent to REM (ie with variable resps and pulse), which may commence instantly on falling asleep, unlike in adults. Hypotonia is normal in REM (stops acting out!); sleep paralysis is seen in 20% of normal people (late return of tone). Benign sleep myoclonus can be very impressive in infants. Only occurs in sleep, baby is otherwise well. There is no other condition like it, so EEG is unnecessary (demonstrate with doll: "That's it!" diagnosis). Nocturnal head banging also common in infants, equivalent to restless legs, can manifest as any sort of rhythmic body rolling. Night terrors care non REM partial arousal episodes, due to an imbalance of sleep/wake drives. Toddler usually, does not recognize parent, lasts 5-10 minutes, happens a maximum of twice in one night, associated with poor sleep habits. Cf frontal lobe epilepsy: brief, starts with a few jerks before waking up upset, can happen 3 or more times a night. Also consider cardiac arrhythmia.
Sleep problems are common in childhood, especially if there are other neurological problems. Consider whether physical needs eg for turning, toileting, pain are contributing. Melatonin appears to help latency, ie getting off to sleep but seems less good at maintaining it. Seems reasonably safe, especially cf other sedatives. Current MENDS trial for use in neurodisability. Various products, none licensed in children for sleep disorders - should only be prescribed by those familiar with its use and after appropriate assessment including sleep diary.
As common as MS. Due to low hypocretin (neuropeptide). Pentad:
Pointers are accidents, mood swings, behaviour change. Ritalin, prednisolone etc not very effective... IVIG has worked for acute onset.
Ask how long it takes to complete a meal.
Pedisure is lactose free, 1 cal/ml.
Erythromycin 2 mg/kg TdS as prokinetic.
No RCTs of gastrostomy feeding in CP. Higher death rates reported, but may be more severely affected children.
Constraint-induced movement therapy (where good limb is constrained by a fibreglass tube) benefits upper arm function in children with hemiparesis.
Sensory disturbances (visual, skin sensitivity/tingling/numbness); ataxia/tremor; cognitive impairment (esp memory, verbal), immune dysfunction. Reversible! Treat with DMSA. Chelation etc offered as treatment for autism, but not really same pattern at all.
One third of children with febrile convulsion/seizure (FS) will experience further FS; age would appear to be the single, strongest, and most consistent risk factor. Most recurrences will occur during the first year after the initial FS and over 90% recur within two years. Other risks - family history of febrile seizures (but not epilepsy) in a first degree relative, children whose initial FS occurred with a relatively low fever, multiple initial seizures occurring during the same febrile episode. Surprisingly, status in an otherwise normal child does not appear to significantly increase the risk for further febrile seizures or the development of epilepsy.
Following a first FS, 2-4% of children will have an unprovoked ie afebrile seizure (4x risk in general population) and most of these children will subsequently develop epilepsy. Other risk factors - family history of epilepsy, complex features, and the presence of early onset neurodevelopmental abnormalities. Genetic basis common but multiple chromosomes, complex! Current opinion supports an association between prolonged FS and pre-existing lesions within the temporal lobe, otherwise no good link between FS and temporal lobe epilepsy.
No indication for EEG or anti-epileptic treatment in febrile convulsions - see SIGN 81.
15% of status epilepticus with fever have meningitis (observational study) - although low rate of LP so underestimate? Fear of LP due to RICP from fit and/or meningitis, so do CT first if in ICU or abnormal neurology else as soon as no contraindication. Treat empirically for meningitis (+/- herpes encephalitis, although risk unknown) with antibiotics and steroids. Chin RFM, Arch Dis Child 2005;90:66-9.(Ed by Kneen)
Risk of dying slightly raised for 2yr after febrile seizure but only for complex ie more than 15min duration or recurrent within 24hr (RR 1.99, but absolute risk v low).(Denmark, Lancet 08;372)
Acute Disseminated Encephalo-Myelitis follows infection, rarely vaccination. A few will recur, and turn out to be MS. Diagnosis is increasing as MRI used more - CT is usually normal. MRI characteristically shows multiple, uniform focal white matter densities, may also affect basal ganglia, cerebellum and spinal cord. In encephalitis, tends to be more diffuse, grey matter and underlying white matter. Lasts weeks to months. Preceding URTI, D&V, immunisation or fever common. Multiple neuro abnormalities including ataxia, speech disorder, cranial nerves esp ocular, mental status. Spinal symptoms and visual loss (1 or both eyes) very suggestive cf encephalitis. Nearly all recover without significant sequelae. Death may result from raised ICP. CSF looks viral: elevated protein, lymphocytic pleocytosis, normal glucose; cultures and enterovirus/herpes PCR are negative by definition. Usually treated with steroids and IVIg, but no evidence. Ped IDJ 2004, J Neurol Neurosurg Psychiatry 2004;75:i10-i15
Diagnosis of exclusion. MRI to exclude spinal compression. Acute onset, maximal within 4hrs suggests anterior spinal infarction (relative sensory sparing). Inflammation seen in CSF. Differential - MS (oligoclonal bands, abnormal VEPs), viral, Guillain Barre (more symmetrical, less bladder/bowel, less pain, vague sensory level, autonomic features). Plateau lasts up to 3 weeks (prognostic). Steroids used, evidence? Rule of thirds - full recovery, mild disability, significant disability.
Truly congenital cf other cerebpal AVMs. Midline, between corpus callosum and cerebellum. Visible antenatally from 26/40; usually neonatal heart failure (ascites, tachycardia, ectopics) else seizures, hydrocephalus. Microcatheter approach with coils & glue. Hydrocephalus is not obstructive - raised venous pressure reduces CSF absorption - so resolves!
VLCFAs high. Bilat white matter changes (T2 MRI bright instead of dark) usually posterior. Rarely adult onset (MS like), rarely Addisons only. X-linked, no genotype-phenotype correlation. 2yr to vegetative state, death up to 10yrs later. Consider BMT for screened cases. Lorenzo's oil not therapeutic but preventive (with diet). Similar Krabbes, Alexander's, Canavans (spongioform).
The 10-year risk of multiple sclerosis following an initial episode of acute optic neuritis is significantly higher if there is a single brain MRI lesion; higher numbers of lesions do not appreciably increase that risk. However, even when brain lesions are seen on MRI, more than 40% of the patients will not develop clinical multiple sclerosis after 10 years. In the absence of MRI lesions, certain demographic and clinical features seem to predict a very low likelihood of developing multiple sclerosis. This natural history information is a critical input for estimating a patient's 10-year multiple sclerosis risk and for weighing the benefit of initiating prophylactic treatment at the time of optic neuritis or other initial demyelinating events in the central nervous system.
For a ventriculoperitoneal shunt to work ie drain CSF effectively from brain to abdomen, there must be a pressure gradient. Hence if shunt malfuntion is suspected, consider shunt fracture/disconnection, blockage, infection (see below), and raised intra-abdominal pressure (eg constipation).
Ventricular shunt infection (VSI) symptoms are nonspecific and may mimic shunt malfunction. Symptoms of infection at the proximal end may include:
Symptoms of distal infections may include abdominal pain, intestinal obstruction or an abdominal pseudocyst (mass).
Other potential features:
Blood tests are pretty unhelpful (except in VA shunts where blood cultures may be positive). A shunt series will check shunt integrity; CT/MRI will identify increased intracranial pressure. USS Abdomen may reveal an abdominal pseudocyst or perforated bowel.
A shunt tap provides the essential information with low risk of introducing infection, although CSF may be abnormal because of underlying disease (eg intraventricular hemorrhage), or from chemical ventriculitis due to bleeding or tissue damage. CSF protein or glucose levels don't help much cf meningitis. Increased CSF eosinophils can be seen in VSI, but also in shunt malfunction. Positive cultures may of course represent colonisation rather than active infection, so correlate with history and examination.
Vancomycin is usually used for gram-positive infections, cefotaxime for gram negatives. Occasionally you get meningitis type bugs ie pneumococcus, meningococcus - can be treated without shunt removal. The antibiotics used must adequately penetrate (ie, >=10x the minimal inhibitory concentration) the blood-brain barrier (BBB) - Vancomycin is not the best at penetrating the BBB (nor are aminoglycosides) so monitoring CSF levels is recommended. Cefotaxime penetrates reasonably well where there is meningeal inflammation but not that well when there isn't - Rifampicin and chloramphenicol are the best, provided the organisms are sensitive. VSI caused by a multidrug-resistant GNR may necessitate treatment with carbapenems or fluoroquinolones. Linezolid penetrates the BBB (limited reports of its use).
In difficult cases consider removal of the shunt with placement of a temporary external ventricular drain (EVD), followed by reinternalization after CSF sterilization. A recent analysis strongly confirmed this as the most effective treatment method. Reinternalization should of course be delayed until CSF sterilization, but it can be performed earlier for CONS compared with other infections. Although it's tempting to delay reinternalization until EVD CSF cultures off antibiotics are negative, waiting the extra days does not appear to reduce the recurrence rate, whereas the risk of new infection correlates strongly with how long the EVD is left in.
Abdominal pseudocysts can be handled differently - they are infected (by culture) in 30-80% of cases; these require only externalization of the abdominal portion of the shunt with reinternalization to a different abdominal quadrant.
Duration of therapy? Depends on bug and presence of CSF changes:
If CSF cultures from EVD remain positive 48 hours after surgery, check trough CSF antibiotic levels, consider replacement. Intraventricular (IT) administration of antimicrobials is controversial: risk of allergic reactions, drug-induced inflammation and toxic or inadequate concentrations. But in resistant cases consider a ventricular antibiotic flush through 2 EVDs (dissolve antibiotic in normal saline to create a safe but therapeutic concentration, infuse at 10-20 mL/hr depending on the rate of CSF production)
Pediatric Infectious Disease Journal. 24(6):557-558
Symptoms appear after 1st year normally. Motor delay - Gower's sign classically ie using arms to stand up from sitting becau.e of poor axial strength. Also associated with learning difficulties, although many normal.
Diagnosis: elevated CK. Usually in the thousands. In late stage disease CK is normal, representing lack of muscle tissue. Necrosis on muscle biopsy.
Steroids work for DMD but ?regimen - either 0.75mg/kg continuous or 10/7 off, 10/7 on. Delays progression for 3yr. Good for preventing scoliosis peripuberty.
SMN1 gene for SMA - multiple copies! Else mutated gene with 10% function (SMN2) - valproate appears to boost transcription in these cases. Gene becomes less important with age so milder forms tend to burn out. The more SMN2 copies, the milder the form. A single functional SMN1 makes you normal.
Delibrate self-harm in adolescents - 1/3 depressed, 1/5 conduct disorder. Social/emotional isolation, abuse very common. 10% risk of recurrence.
Psychosis - differential diagnosis: encephalitis, encephalopathy (hashimoto's reponds to steroids), Sydenhams/pandas (esp with OCD, tics, emotional lability).
Severe learning difficulty= IQ35 or less, expected mental age 5yr at best.
Glasgow has an evidence based pathway for investigation.
History: family history, pregnancy (drugs, threatened miscarriage, neonatal encephalopathy).
Examination:
Investigations:
Second line tests:
Archives of Disease in Childhood 2006;91:701-705. PMID 16861488
Better name is Idiopathic intracranial hypertension, since not entirely benign...
The diagnosis is made when intracranial hypertension is found but with normal CSF, and no ventriculomegaly. Usual symptoms of early morning headache, effortless vomiting. VI palsy may be seen, rarely IIÍ/IV. Papilloedema is often the first clue.
No sex differential prepubertally, not associated with obesity.
Normal CSF opening pressure is 7.5cm of water <2yr, 13.5 <5yr, 20 over 5yr. Lumbar puncture is therapeutic; 2 step tap procedure is usually used if opening pressure is over 30cm. NB General anaesthetic can give false pos result! Secondary causes include drugs, endocrine conditions.
Since repeated LP is unpleasant, medical therapy can be considered. Topiramate is probably equivalent to the more usual acetazolamide (a diuretic). Steroids should be used for malignant hypertension (ie where there is rapid progression). Any of these treatments may result in a low pressure headache.
Surgical options include Optic nerve sheath fenestration, lumbar-peritoneal shunt.
An acute inflammatory demyelinating polyradiculopathy, almost certainly autoimmune since antibodies to ganglioside are often found (GQ1b in particular is highly sensitive and specific for Miller-Fisher syndrome = ophthalmoplegia with ataxia & absent reflexes). Some cases are purely motor, others are mixed. About a quarter follow Campylobacter infection, and there is clear homology between epitopes and gangliosides. Strongly associated with HIV in the tropics.
Usually gradual onset over a few days but rarely can be over a few hours. Presents with pain, numbness, paraesthesiae, weakness. Weakness may initially be proximal or distal (distal alone suggests a withering axonopathy eg toxin). Facial nerves often affected. Reflexes usually lost early but sometimes persist (ie axonopathy rather than radiculopathy). Autonomic features may occur eg urinary retention, sinus tachycardia, ileus. The degree of paralysis can be extreme - up to 20% require ventilation. Monitor respiratory ability serial peak flows. Gradually worsens, peaks at around 2 weeks (by definition, within 4 weeks). Then there is a variable plateau phase. 20% will have persisting disability; fatigue is common.
The diagnosis is often pretty obvious but investigations should be done to rule out other causes. If purely motor, differential includes hypokalaemia, polio, myasthenia gravis, botulism, acute myopathy.
Consider also:
The initial progressive phase lasts 10-30 days. If deterioration continues beyond four weeks, the diagnosis of GBS is pretty much excluded - suggests chronic inflammatory polyneuropathy (CIDP). In rapid, aggressive disease complete quadriplegia can develop in 2–5 days; usually severe respiratory involvement with ventilatory failure, and autonomic involvement placing them at risk of life-threatening arrhythmias and hypertension. Aspiration pneumonia is another major risk.
Children should be admitted to PICU if they have:
Plasma exchange is gold standard. Surprisingly, steroids do not appear to have any benefit (cf CIDP), as they can sometimes make things worse or slow the recovery. Perhaps nerve damage at presentation is already programmed/complete? Or do they impair healing? IVIG 0.4g/kg for 5 days (started as soon as possible and ideally within first 2 weeks, although benefit may extend up to 4 weeks) is as effective as plasma exchange (in adults, Cochrane) and probably quicker as well as safer. In kids, 250 ml/kg volume exchange or roughly a triple-volume exchange probably best. The conventional dose of immunoglobulin is a total of 2 g/kg. Some protocols for GBS have suggested 0.5 g/kg/day for four days or 1.0 g/kg/day for two days.
For pain which is resistant to conventional analgesia, gabapentin and carbamazepine may be useful.
Mortality in childhood GBS is less than 5%. Deaths may be caused by ventilatory failure (rare now), cardiac arrhythmias, dysautonomia and pulmonary embolism. Full recovery within 3–12 months is experienced by 90–95% of children with GBS; that leaves 5-10% with permanent neuro deficits, but most of those tend to have only minor disability.
PMID 18032711
Tics are recurrent, sudden, non-rhythmic twitches. Can be in 1 muscle or muscle group, but can also be a more complex semi-purposeful movement, or even a bizarre gait. Tend to be situational, with stress making them worse. Initially they are suppressible, although depending on the situation this suppression can be virtually effortless! Usually though, suppression leads to rising anxiety and then a rebound in frequency. There is often a premonitory feeling. They can be suggestible. Although tics can wax and wane over time, there is a general tendency to improve, and they are very unusual in adulthood.
Tics occur most commonly in boys. Usually they are transient, lasting for between 4 weeks and 1 year. A chronic tic disorder does exist distinct from Tourettes.
Tourette's syndrome is thought to affect 1% of children, although in many cases it does not seem to cause any significant problems! Starts at a mean age of 7 but can be as young as 2yrs. Motor tics come first, about a year before vocal tics. The other characteristic features of Tourettes are:
Obscene language is not essential. In some patients, there is a non-obscene compulsion to shout socially inappropriate things.
Differential is brain injury eg post-encephalitis, Huntingtons.
Pure tic disorder is unusual in Tourettes. The commonest comorbidities are:
The comorbidities are often more significant on school performance than the tics.
Counselling is useful for self-esteem, anger management, and social functioning. Habit Reversal Training is effective but not widely available. Drug treatment is tailored around symptomatology, but usually involves traditional or atypical neuroleptics, or clonidine.
Stern, Curr Peds 2006:16:459
A syndrome of agitation, sweating, flushing in association with a spinal cord lesion. Most commonly, a strong sensory stimulus below the level of the lesion eg urinary retention, bowel distension evokes a massive reflex sympathetic surge. Normally cerebral vasomotor sensors would inhibit but are blocked by the spinal lesion. Effects are:
Mostly seen in men! Other triggers can be lower limb pain.
Management:
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