Radiological imaging of parkinsonism. Dr/ ABD ALLAH NAZEER. MD.
Parkinson's disease described by James Parkinson in 1817. Parkinson’s disease is a chronic neurodegenerative movement disorder affecting voluntary and emotional movements and most commonly seen in the elderly, but is also found in the young and inexorably progresses leading to significant disability. Average age of onset is 62.5 years. Men and women affected equally. Pathogenesis: Four theories. Oxidative damage , Mitochondrial dysfunction, enhanced oxidative stress, proteosomal dysfunction causes cell death. Environmental toxins , MPTP-Methyl-phenyl tetrahydropyridine, Mutation in the gene located on chromosome 4. Genetic predisposition , Mutation in the gene located on chromosome 4. Accelerated aging.
Classification and Etiology. Idiopathic Parkinson’s disease Parkinson-like syndromes Drug induced parkinsonism Hypoxia Tumor Trauma Vascular:Multiinfarct Toxin:Mn, CO, MPTP and cyanide Post-encephalitic parkinsonism (von Economo’s encephalitis) Normal pressure hydrocephalus Wilson’s disease, Hutington’s disease
Medications that can cause parkinsonian symptoms, but not PD itself, include the following: Metoclopramide Domperidone Reserpine-containing antihypertensives Neuroleptics Some evidence also indicates that certain environmental factors (including smoking and coffee drinking) may actually have protective associations.
Clinical features of Idiopathic Parkinson’s disease. Major features Resting tremor in hands, arms, legs, jaw, and Face. Bradykinesia Rigidity- cogwheel or lead-pipe Minor features Bradyphrenia Speech abnormalities Depression Dysautonomia Dystonia Constipation Hallucinations Dysphagia
Parkinson’s disease Symptomatology.
Tremor dominant Tremor: Rest Fixed frequency 3-6 Hz Not a feature of old age Pill-rolling Usually starts in one limb, and then to other limbs Rarely starts in lower limbs Intermittent for many years They usually disappear briefly during movement and do not occur during sleep . Tremors can also eventually occur in the head, lips, tongue, and feet. In younger patients tremor is usually predominant and often suggests a less aggressive form of the disease .
Rigidity Striatal hand : Ulnar deviation, MCP flexion, IP extension Striatal toe : Big toe dorsiflexion Sitting en bloc : Collapses into a chair on attempting to sit down Posture Kyphosis Flexed elbows, knees and hips Hands held in front of body Trunk bent forward Head bowed
Bradykinesia Slowness of motion (bradykinesia) is one of the classic symptoms of Parkinson's disease. Hypomimia- “masked facies ”, expressionless face, blinking Speech abnormalities- Hypophonia: soft voice Aprosody of speech: monotonous and lack of inflection Tachyphemia: do not separate syllables together, running words together Patients may eventually develop a stooped posture and a slow, shuffling walk. The gait can be erratic and unsteady.
Motor fluctuations Freezing phenomenon- Sudden, transient inability to perform active movements, lasting no more than a few seconds: Start hesitation Turn hesitation Target hesitation Palilalia (speaking) Apraxia of eyelid opening Writing Kinesia paradoxica-Despite severe rigidity and bradykinesia, they may rise suddenly and move normally.
Investigations: The diagnosis is made clinically , as there is no diagnostic test for Parkinson's disease. Imaging (CT or MRI) of the brain needed if there are any features suggestive of pyramidal, cerebellar or autonomic involvement or the diagnosis is otherwise in dought (e.g to exclude stroke). Routine brain imaging is unnecessary in patients with typical Parkinson’s disease. Dopamine transporter (DAT) imaging can help to differentiate patients with Parkinson’s disease from healthy individuals and patients with essential tremor or drug induced parkinsonism Structural MRI may be performed to rule out alternative diagnoses (including other neurodegenerative syndromes and structural or vascular lesions ).
T1-weighted MR images show bilateral and symmetrical hyperintensities in the substantia nigra and cerebral peduncle (A), subthalamic region and hemispheric white matter (B), and the globus pallidus and putamen (C ) in reversal parkinsonism patient following embolization of intra-hepatic venous shunt.
19-year-old man with secondary parkinsonism (carbon monoxide intoxication) 3 years after onset, with hyperintense lesion at the globus pallidus and atrophy of the substantia nigra.
Parkinsonism due to predominant involvement of substantia nigra in Japanese encephalitis
A 64-Year-Old Woman With Bradykinesia and Rigidity in epilepsy.
Reversible Acute Parkinsonism and Bilateral Basal Ganglia Lesions in a Diabetic Uremic Patient.
Differential diagnosis of parkinsonism using brain 18 F-FP-CIT PET. Brain PET/CT images of 18 F-FP-CIT uptake at level of striatum demonstrate different DAT density in different conditions. DAT density is decreased in PD patient (B), whereas DAT density is normal in healthy subject (A) and in patients with drug-induced parkinsonism (C) and essential tremor ( D).
Color-coded diffusion-weighted MRI and (B) striatal 123I-2β-carbomethoxy-3β-(4-iodophenyl)-N-(3-iodophenyl ) tropane uptake for a healthy individual, a patient with Parkinson’s disease (PD), and a patient with the atypical parkinsonian syndrome multiple system atrophy (MSA). The apparent diffusion coefficient (A) is normal in the striatum in PD but it is raised in MSA (arrows) because of the neuronal loss that targets the putamen. Dopamine transporter binding (B) is bilaterally reduced in the striata in both PD and MSA. In PD, the caudate is relatively spared compared with the putamen.
White matter lesions in Parkinson disease
Fluid-attenuated inversion recovery magnetic resonance imaging sequence of the brain in a patient with West Nile virus encephalitis with associated parkinsonism and tremor, displaying signal abnormality in the substantia nigra (short arrow), the mesial temporal lobe (long arrow) and right posterior thalamus (thick arrow).
Dual-Tracer Dopamine Transporter and Perfusion SPECT in Differential Diagnosis of Parkinsonism Using Template-Based Discriminant Analysis
Abnormal signal within the Substantia Nigra in Parkinson Disease.
Abnormal signal within the Substantia Nigra in Parkinson Disease.
Parkinson Disease with abnormal signal within the pars impacta at the substantia nigra.
Left: an axial section through an averaged multispectral image at the level of the midbrain showing the substantia nigra (SN) in a healthy control participant. Right: magnified view of the SN in a healthy woman (top) and a woman with Parkinson disease (PD) (bottom); signal loss in the SN is striking in the PD brain (green arrow).
Magnetic Resonance Imaging (MRI) in Parkinson′s Disease.