Certain imaging techniques are suited to certain situations, eg, doppler ultrasound or MRA to assess the carotids; CT to exclude bleeds; T2* sequences on MR to assess microbleeds; diffusion-weighted sequences for acute lacunar infarcts, etc, etc, etc. Was the most appropraite imaging used based on the clinical signs?
What do you mean by discrepancy of clinical signs and neuroimaging findings? What imaging modality are you comparing to (CT, MR)?
Clinical signs are the consequence of biochemical processes which do not necessarily generate contrast in imaging techniques. MRI, for example, generates contrast based on relaxation and proton density. These mechanisms are independent of pathologies of diseases. On the occasions when biochemistry of the pathology causes changes in relaxation and water content, then MRI gains sensitivity for visualization of that particular pathology.
The neurological examination (detection of clinical signs) is not elaborate enough to find any disturbance of brain function. The functions of the brain are far too many. A neuroimaging finding might refer to a "function" of the brain that we would regard as "personality" for example. And "personality" changes constantly anyway. It might differ because we are hungry, tired, in love, .... - or because one has developed a brain lesion. We were very surprised to see many, many clinically "silent" DWI lesions in acute stroke patients:
Incidence of new diffusion-weighted imaging lesions outside the area of initial hypoperfusion within 1 week after acute ischemic stroke.
Usnich T, Albach FN, Brunecker P, Fiebach JB, Nolte CH.
Stroke. 2012 Oct;43(10):2654-8.
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Silent new DWI lesions within the first week after stroke.
Nolte CH, Albach FN, Heuschmann PU, Brunecker P, Villringer K, Endres M, Fiebach JB.
Cerebrovasc Dis. 2012;33(3):248-54.
Are you referring to a patient in particular? Can you add more details?
Generally speaking, neuroimaging can be not sensible enough to identify the lesion responsible for clinical signs, but it depends on several factors, such as the timing of the examination respect to symptoms onset, the selection of the right tecnique for that patient. Sometimes you have to consider also others factors, such as hydroelectrolytic/metabolic imbalance and/or non convulsive seizures complicating severe strokes, that can modify clinical presentation.
This paper discusses synaptic damage after stroke and that MRI scans are not sensitive to it:
Ischemic Cerebral Damage An Appraisal of Synaptic Failure, J Hofmeijer, MJAM van Putten - Stroke, 2012
In stroke imaging,first thing is what imaging we are reffering at( CT or MR)?second is (,when after stroke ),the imaging was done as the changes refelected are based on pathophysiological changes.On the other hand ,it is also not unsual to find clinically silent lesion on imaging as referred by others also.we need probably more sensitive technique to assess the microcellular damage .
Maybe it would be useful to refer to the neurosurgical concept of "eloquent brain areas". Most of our symptomatology refers to brain areas like the motor system or primary sensory systems. Behavioral systems are difficult to assess. Maybe for several reasons: (1) brains are individual, it depends on which brain is lesioned, i.e. the premorbid status. (2) some lesions are only clinically detected when asking proxies, and than one depends on the proxies' perception. (3) some of the lesions escape detection, notorious for MRI-negative stroke of the lower brainstem. (4) the ischemic lesion is dynamic due to metabolic reasons, later on because of compensation. (5) consider stroke mimics, i.e.. migraine or epilepsy with negative features.
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