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Individual differences |
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"All went lame; all blind; Drunk with fatigue; deaf even to the hoots Of tired, outstripped Five-Nines that dropped behind." Wilfred Owen (Dulce et Decorum Est"
Many patients (40%) present to neurologists with a variety of symptoms for which there is no current organic or psychological explanation despite extensive investigation.
The diagnosis of Functional Neurological Deficit provides an umbrella term for a variety of symptoms of apparent neurological origin but which current models struggle to explain psychologically or organically. Presentation may be similar to a wide range of other neurological conditions from paralysis to weakness.
Functional Neurological Deficit can present with any motor or sensory symptom in the body including:
- Weakness / Paralysis of a limb or the entire body Impaired hearing or vision
- Loss / Disturbance of sensation
- Impairment or loss of speech
- Fixed Dystonia unlike normal dystonia
- Tremor, Myoclonus or other movement disorders
- Gait Problems
Given the occurrence of these medically unexplained symptoms in patients with organic brain injury, spinal injury, to post-anaethaesia and post-viral illnesses, the modern term moves away from psychodynamic theory and provides a useful label for what is a complex and little understood disorder.
Abnormalities in orbitofrontal, cingulate or prefrontal cortex circuits in processing environmental stimuli from the CNS result in an interruption of “awareness” of contralateral basal ganglia and thalamic motor-circuits. Once the connection is disrupted motor circuits are no longer activated by cortex activity as they rely on reciprocal paths for continual function. In effect it is a hardware crash caused by an interruption of power (consciousness) with a corresponding decrease in blood flow to the basal ganglia and thalamus.
Macrocosmic damage (in the form of lesions for example) in the same subcortical pre-motor circuits may also result in unilateral motor neglect, where voluntary limb use may fail despite a lack of true paralysis and intact primary sensorimotor pathways.
As such hypothesised perpetuating aetiologies and even the precipitating stimuli are relatively unimportant, certainly psychodynamic theories of primary and secondary gain are of questionable relevance . Symptoms may indeed arise in any circumstance that the cortex is not structurally equipped to deal with; from post-anaesthetic weakness, neurological damage , viral infection, fatigue to trivial psycho-social events . These are not however the cause of symptoms but rather the abnormalities within the cortex predispose the brain towards a systemic reaction. (think about how windows randomly crashes) Hence a history of functional symptoms may me be found in individuals. In other species the prefrontal cortex is dedicated to voluntary movement but in man it's development encompasses a variety of higher functions including memory and imagination.
As Functional Deficits arise almost certainly from the brain's idea of a limb (stone) then it is useful to hypothesise that dysfunction in the prefrontal cortex has caused the disconnection downstream (Vuilleimier) with the observation of prolonged phsyiotherapy being that patients "have forgotten how to move properly". Other prolonged observations showing "that patients have real changes of tone" is also thus explained by reciprocal motor neglect.
As the prefontal cortex is also associated with a variety of psychological deficits co-existing disturbances of consciousness and mood may also be present though co-morbidity is not a necessary precursor to functional motor symptoms.
Treatment options should be aimed towards the re-establishment of power (consciousness) to affected motor circuits through explanation of the condition, proprioception based physiotherapy and drug treatment.
The importance of the sub-cortex in movement and its relatively recent evolution could be hypothesised as the structural flaw in the “animal who knows and knows that he knows.” Chardin Studies of functional symptoms in other higher mammals thus offer the possibility of further insight into what is a distressing and often long-term, though completely reversible condition.
- As below also Hurst
- Vuilleumier P, Chicherio C, Assal F, Schwartz S, Slosmen D, Landis T. Functional neuroanatomical correlates of hysterical sensorimotor loss. Brain 2001; 124: 1077–90 & Yazici KM, Kostakoglu L. Cerebral blood flow changes in patients with conversion disorder. Psychiatry Res 1998; 83: 163–8
- See “The psychology of the senses and their functional disorders”- Arthur Hurst (croonian Lectures) for an aetiology based on “suggestion” and “attention & volition”
- Eames P. Hysteria following brain injury. J Neurol Neurosurg Psychiatry 1992; 55: 1046–53
- Freud, Dreams and their interpretation (for the psychodynamic theory linking recent trivial events to past trauma, see Webster “Why Freud was Wrong” for analysis of this theory) The essential feature of a conversion disorder is a loss of,or alteration in,physical functioning that suggests a physical disorder but which instead is an expression of a psychological conflict or need. See Webster for a rebuttal of this. Also Hurst & Charcot ie- Le Log.
- Hurst (as above)
- Carson AJ, Ringbauer B, Stone J, et al. Do medically unexplained symptoms matter? A prospective cohort study of 300 new referrals to neurology outpatients. J Neurol Neurosurg Psychiatry 2000;68:207–10