Archive for the ‘Demenz/Atrophie’ Category

Metachromatische Leukodystrophie(MLD)

Sonntag, 06. Mai 2018

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Mittwoch, 18. Januar 2017

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Freitag, 25. September 2015
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Vd.a. progressive supranukleäre  Parese, subjektiv orientierend Symptomfrei. (Symptombeginn oft mit 50-60 Jahren).

Neurologisches Konsilium folgt.

(Kolibri-Zeichen,Humming-bird sign,Mikeymous Zeichen,Atrophie)

Swallow Tail Sign Parkinson

Dienstag, 30. September 2014

The ‘Swallow Tail’ Appearance of the Healthy Nigrosome
– A New Accurate Test of Parkinson’s Disease: A Case-
Control and Retrospective Cross-Sectional MRI Study at






Neuro_ROI Auswert_Software:


The Swallow tail sign : Parkinson mit CMRT Diagnostizieren !!!
A. High resolution SWI MRI (3D gradient echo EPI, magnitude image)
B. Clinical high resolution 3D-T2*/SWI MRI (Philips ‘PRESTO’ sequence),
In the retrospective study, MR imaging was performed on the same scanner as above, also with a standard eight-channel head coil, using a standard clinical Phillips ‘Principles of Echo Shifting with a Train of Observations’ (PRESTO) sequence. PRESTO is a HR-T2*/SWI 3D multi-shot fast field echo – echo planar imaging sequence FFE-EPI. TR/TE 16.55/23.29, echo train length 1, Flip angle 10°, number of slices: 200, voxel size 0.43×0.43×0.75 mm3, SENSE factor 2, Scan duration: 2 minutes 36 seconds). The orientation of acquired axial slices was in alignment with the splenium and genu of corpus callosum in the sagittal plane.


M. Parkinson(Neuroimaging)

Sonntag, 10. August 2014


(Siehe auch CMRT neurodegenerative Erkrankungen)

The first step involves the confirmation of symptoms necessary to make a diagnosis of parkinsonism, which includes the presence of bradykinesia, defined as slow initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions, and the presence of either muscular rigidity, a 4-to 6-Hz rest tremor, or postural instability not caused by visual, vestibular, cerebellar, or proprioceptive dysfunction.

The second step involves the identification of criteria that would exclude a diagnosis of PD including history of repeated strokes with stepwise progression of parkinsonian features (suggestive of vascular parkinsonism); history of repeated head injury (suggestive of pugilistic parkinsonism) or definite encephalitis, oculogyric crises; neuroleptic treatment at onset of symptoms (suggestive of drug-induced parkinsonism [DIP]); more than 1 affected relative; sustained remission; strictly unilateral features after 3 years; supranuclear gaze palsy (suggestive of progressive supranuclear palsy [PSP]); cerebellar signs; early and severe autonomic involvement (suggestive of multiple system atrophy [MSA]); early and severe dementia with disturbances of memory (suggestive of dementia with Lewy bodies [DLB]), language, and praxis (suggestive of corticobasal ganglionic degeneration); Babinski sign; presence of cerebral tumor or communicating hydrocephalus on CT scan; negative response to large doses of levodopa (if malabsorption excluded); and exposure to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).

Finally, the third step is to identify at least 3 of the following supportive criteria for the diagnosis of PD: unilateral onset, rest tremor, progressive disorder, persistent asymmetry affecting side of onset most, excellent response (70%-100%) to levodopa, severe levodopa-induced chorea, levodopa response lasting at least 5 years, and a clinical course of at least 10 years.

Although PD is the most common cause of parkinsonism, multiple disorders include features of parkinsonism, which can make the differential diagnosis of PD a challenge (Table 1). The disorders most commonly confused with PD include essential tremor (ET), MSA, PSP, corticobasal degeneration (CBD), DLB, DIP, vascular parkinsonism, and psychogenic parkinsonism.

Essential Tremor

ET affects an estimated 10 million people in the United States and is one of the movement disorders most commonly confused with PD. ET can occur at any time throughout the lifespan; it is often associated with a strong autosomal dominant family history of tremor. In contrast to PD, ET involves the presence of postural and kinetic tremor with the absence of bradykinesia and rigidity. In addition, a reduction in tremor often occurs with ingestion of alcohol, tremor onset is typically bilateral, handwriting is large and tremulous, tremor often occurs in the head and/or voice, and tremor is the predominant symptom

Multiple System Atrophy

MSA is a neurodegenerative movement disorder; approximately 80% of cases have a predominantly parkinsonian form (MSA-P) and 20% have a cerebellar form (MSA-C). Early in the disease course, MSA can be indistinguishable from PD. However, MSA generally progresses more quickly, presents in the early 50s, and has a shorter disease course than PD.[15,16] Early autonomic symptoms are common and include orthostatic hypotension, urinary incontinence, and erectile dysfunction. MSA typically does not have a good response to levodopa; however, early in the disease course, an initial response to levodopa may be observed, but it is rarely sustained(—> CMRT)

Progressive Supranuclear Palsy

PSP is a neurodegenerative form of parkinsonism. The presenting symptom of PSP is often postural instability with associated falls, which has been shown to be one of the strongest predictors of a PSP diagnosis.[19] Another strong predictor of this disorder is vertical supranuclear palsy with downward gaze abnormalities.[20] Early and often significant cognitive changes, apathy, and disinhibition, as well as speech and swallowing problems are common with PSP. The onset of PSP tends to be symmetric, usually with minimal to no rest tremor, gait may be wide-based and ataxic, the response to levodopa is poor, and PSP generally progresses more quickly than PD. Rigidity tends to be greater in the neck than the limbs and it is not uncommon to see an extended posturing of the neck(—> CMRT)

Corticobasal Degeneration

CBD is one of the least common neurodegenerative forms of parkinsonism. It is a slowly progressive, asymmetric disorder with the core features of rigidity and apraxia, and a poor response to levodopa.[22] Varying degrees of cognitive dysfunction may also be present.(—> CMRT)

Dementia with Lewy Bodies

DLB accounts for up to 20% of all cases of dementia and can be difficult to differentiate from PDD and from AD.[24] The most common features are hallucinations, parkinsonism, and fluctuating attention. The diagnosis is generally DLB if dementia and parkinsonism occur within 1 year of each other, PDD if dementia occurs more than 1 year after parkinsonism, and AD when significant dementia occurs early with minimal to no parkinsonism at presentation.[25,26] In addition, parkinsonism is generally symmetric, whereas early gait and balance issues are common in DLB. Dementia primarily involves executive and visuospatial function in both DLB and PD, but it generally occurs early in DLB and late in PD. By contrast, early and severe memory impairment is seen in AD.[26] In addition, autonomic dysfunction may be present early in DLB, occurs much later in PD, and is rare in AD. Visual hallucinations are most common in PDD, less common in PD, and least common in AD. Finally, PDD has a strong response to levodopa, DLB has a less consistent response to levodopa, and AD has no response to levodopa(—> CMRT)

Drug-Induced Parkinsonism

DIP is the most common cause of secondary parkinsonism and generally results from the use of neuroleptics, antiemetics, and other dopamine blocking drugs. Its onset is generally acute, bilateral, and symmetric. Bradykinesia is the most common feature but rigidity, tremor, and gait abnormalities may also be present. DIP also tends to occur more often and to be more severe in older persons. In most cases, DIP is reversible and resolves within weeks to months after the offending agent is discontinued. The first step in the diagnostic process is to review the medication history and discontinue any potential causes of DIP

Vascular Parkinsonism

No specific diagnostic criteria have been formulated for vascular parkinsonism. However, studies have been conducted to identify key features and risk factors.[28] Cerebrovascular disease and risk factors have been shown to be significant features for differentiating vascular parkinsonism from PD. In addition, when compared with PD patients, those with vascular parkinsonism tend to be older, more often present with gait difficulty, often have predominantly lower body symptoms with postural instability and falling, and are more likely to have dementia, incontinence, and pseudobulbar affect. Bradykinesia and rigidity are common, but tremor is generally not present. Onset is typically sudden with stepwise progression. In addition, vascular parkinsonism usually responds poorly to levodopa.(—> CMRT)

Psychogenic Parkinsonism

Psychogenic parkinsonism is relatively rare compared with other psychogenic movement disorders but can at times be difficult to differentiate from PD.[29] No specific guidelines have been developed for the diagnosis of psychogenic parkinsonism. Key features include the resolution of symptoms with distraction or use of a placebo medication, task, or test. In addition, tremor generally has variable frequency and amplitude that tends to take on the frequency of other movements.


SPECT of patients with early PD shows an asymmetric reduction in dopamine transporter density that is greatest in the putamen, mild to normal in the caudate, and greatest contralateral to the most affected side of the body. In several studies, SPECT successfully differentiated PD/parkinsonism from ET with a sensitivity ranging from 87%-98% and a specificity ranging from 80%-100%. In these cases, the majority of the patients with PD had a reduction in dopamine transporter (DAT) density whereas the SPECT images for ET and control subjects were normal.

The Parkinson plus syndromes, MSA, PSP, CBD, and DLB, cannot be reliably differentiated from PD with SPECT because all have putamenal DAT reduction; however, it has been suggested that the caudate and putamen are more equally affected in the Parkinson plus syndromes and putamenal DAT exhibits a more symmetric reduction.[49,50] SPECT can however, be useful in differentiating DLB from AD, as DLB has a reduction in putamenal DAT whereas SPECT in AD is normal.[51,52] Studies have shown that SPECT can successfully differentiate DLB and AD with a sensitivity of up to 78% and specificity of up to 94%.

Positron Emission Tomography

PET is also a functional imaging technique and has higher resolution compared with SPECT; however, PET is more costly and is not widely available. A radioactive isotope, commonly 18fluorine or 11carbon, is attached to a compound, commonly DOPA or deoxyglucose, such that the binding and metabolism of the compound can be measured.[34] 18fluorine-DOPA is a marker of the striatal presynaptic dopaminergic terminal DOPA decarboxylase activity and can differentiate PD and other forms of degenerative parkinsonism from controls because parkinsonian patients have significantly less putamenal uptake. In addition, asymmetry is seen in patients with PD but not controls; the uptake in the caudate and putamen is about equal in controls, but patients with PD have an approximate 50% reduction in the putamen and a 10% reduction in the caudate.[55]

As with SPECT imaging, differentiation of various forms of parkinsonism is not reliable.

Transcranial Sonography

Multiple studies have shown a hyperechogenicity of the substantia nigra in up to 90% of patients with PD regardless of disease severity.[70-71] However, increased echogenicity is also seen in the substantia nigra of patients with DLB, CBD, and 9% of normal controls. The sensitivity of identifying PD was 48%-100% across 31 studies.

The limitations of this technique include the inability to complete the testing if the bone window is insufficient, potential variability of outcomes based on the equipment used and the interpreter, and currently limited follow-up and small sample sizes in the majority of the reported studies. The advantages of this technique are that it is less costly than other imaging techniques, and it is widely available, fast, easy to administer, and mobile. Further research is necessary to confirm the clinical utility of this technique in the differential diagnosis of PD.


The differential diagnosis of PD can be challenging and often cannot be determined based on clinical features alone. According to several diagnostic guidelines,[9-11] various neuroimaging techniques can be useful in the diagnosis of difficult cases in combination with published diagnostic criteria and the clinical judgment of a movement disorder specialist. At this time, SPECT imaging is most useful in differentiating PD from ET and nondegenerative forms of parkinsonism including psychogenic, drug-induced, and vascular parkinsonism, and for differentiating DLB and PD dementia from AD. MRI can rule out structural or ischemic lesions and can be useful in identifying vascular parkinsonism. There is also some evidence that MRI can differentiate between PD and MSA and also among the various Parkinson plus syndromes, based on the degree and distribution of atrophy. At this time, there is not enough evidence to recommend advanced MRI techniques, PET, or TCS in the differential diagnosis of parkinsonism, although each is promising; further study will determine their utility in diagnosing PD and related disorders



Montag, 25. November 2013




Alzheimer/Demenz Therapie

Samstag, 15. Oktober 2011

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Donnerstag, 12. Mai 2011

[flagallery gid=4 name=“Gallery“]


Bildinformation: i Anklicken !

Nur vorübergehend aus urheberrechtlichen Gründen zu Testzwecken zugänglich.

Zitiert aus der Radiologe u.a. . Work in progress.

Zur Demonstration einer Bildreferenzdatenbank.

Neurodegenerative Erkrankungen

Freitag, 09. Mai 2008


Neurodegenerative Erkrankungen (Checkliste)

Atypische Parkinson-Syndrome haben zurzeit eine weitaus ungünstigere Prognose und sprechen kaum auf eine dopaminerge Medikation an. Eine möglichst frühzeitige differenzialdiagnostische Abgrenzung der atypischen Parkinson-Syndrome gegenüber dem idiopathischen Parkinson-Syndrom ist von erheblicher klinischer Relevanz. Im Falle der künftigen Entwicklung kausaler, neuroprotektiver Therapiestrategien wird eine frühe Diagnose einen rechtzeitigen Therapiebeginn ermöglichen. Im Frühstadium können die Multisystematrophie, die progressive supranukleäre Blickparese sowie die kortikobasale Degeneration vom idiopathischen Parkinson-Syndrom schwer zu unterscheiden sein.

The same brain regions that undergo atrophy in Alzheimer’s disease are also seen in cognitive decline related to Parkinson’s disease (PD), a new study shows.

Atrophy in the hippocampus and temporal and parietal lobes, and decreased volume in the prefrontal cortex, is evident in patients with PD who have cognitive impairment, including those with only mild cognitive impairment (MCI), investigators observe.

The main differential diagnostic consideration in DLB is Parkinson disease dementia (PDD), because the clinical features of DLB are very similar to those of PDD.

The diagnosis of probable DLB requires progressive cognitive decline/dementia and at least 2 of 3 core features: fluctuating cognition, visual hallucinations, and spontaneous parkinsonism. Other suggestive and supportive criteria include dysautonomia, REM sleep disorder, neuroleptic sensitivity, depression, delusions, and other (nonvisual) hallucinations. In the absence of 2 core features, the diagnosis of probable DLB can also be established if the patient has 1 core feature with at least 1 suggestive feature (REM sleep disorder, neuroleptic sensitivity, single-photon emission CT or PET scan with low dopamine transporter uptake in the basal ganglia). The present case fulfills the diagnostic criteria for probable DLB, with 3 core features and 3 supportive features (orthostatic hypotension, auditory hallucinations, and depression).

Lewy bodies (Medscape) vs. Parkinsondemenz:


Donnerstag, 24. Januar 2008




Pontocerebelläre Atrophie mit Vd a. MSA-C.65 jahre,Ataxie, expansive Lipome

im Bereich der Hand und suboccipital.


Xanthome und Sehnenschwellungen (zerebrotendinöse Xanthomatose),
Zerebrotendinöse Xanthomatose
Zerebrotendinöse Xanthomatose Sterol-27-Hydroxylase Cholestanol erhöht. Die zerebrotendinöse Xanthomatose wird mit Chenodeoxycholat (750 mg/d p.o.) () (Berginer et al. 1984) und einem Statin, z. B. Simvastatin oder Lovastatin () (Peynet et al. 1991) behandelt. Durch diese Behandlung kommt es zu einem deutlichen Abfall der Serumspiegel von Cholestanol. Die weitere Progression der neurologischen Symptome, nicht jedoch von Katarakt und Sehnenschwellungen, kann so verhindert werden.

Verlauf innerhalb von 4 Jahren nach Voruntersuchung.


Olivopontocerebellare Atrophie: 70 Jahre weiblich, Ataxie und Fallneigung:

IMG-0001-00001 IMG-0002-00001


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