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Biomedical subjects

Andrea Radtke

Publications and source records attributed to Andrea Radtke.

5 recordsLinked to original sources
PubMed2004

Migrainous vertigo presenting as episodic positional vertigo.

Migraine can cause vestibular symptoms including positional vertigo. Of 362 consecutive patients presenting with positional vertigo, 10 with migrainous vertigo mimicking benign paroxysmal positional vertigo (BPPV) were identified. The following factors help to distinguish migrainous positional vertigo from BPPV: short-duration symptomatic episodes and frequent recurrences, manifestation early in life, migrainous symptoms during episodes with positional vertigo, and atypical positional nystagmus.

Age of Onset↗
PubMed2003

Venous drainage patterns in a case of pseudotumor cerebri following unilateral radical neck dissection.

We report the extracranial venous ultrasound findings in a case of pseudotumor cerebri (PTC) following unilateral radical neck dissection (rND). PTC is known to be a rare complication following bilateral rND, and is caused by venous outflow obstruction. Single cases of PTC have been reported after unilateral rND, and are thought to be due to resection of the dominant internal jugular vein (IJV) in the presence of a hypoplastic or aplastic contralateral transverse sinus. Our patient developed PTC despite prominent flow in the contralateral IJV as shown by venous ultrasound. No compensatory increase in flow in the vertebral veins was observed, as confirmed by digital subtraction angiography. We conclude that the physiological collateral function of the vertebral venous system and deep neck veins was insufficient and contributed to global venous outflow obstruction in our case of unilateral rND.

Humans↗
PubMed2003

Vestibulo-autonomic control in man: Short- and long-latency vestibular effects on cardiovascular function.

We examined the hypothesis that vestibular signals may exert a rapid control on the heart adjusting cardiovascular function to maintain homoestasis during changes in body posture. Short- and long-latency effects of vestibular stimulation on heart rate (HR), systolic blood pressure (SP), diastolic pressure (DP) and digital blood flow (BF) were studied in fourteen normal controls (NC) and nine labyrinthine-defective subjects (LDS) exposed to abrupt head accelerations. Subjects lay supine with their head suspended in a sling whose 'release' was triggered at delays of 170 ms and 570 ms after an R-spike of the ECG. Release caused the head to fall with an acceleration approximately 0.8 g for approximately 140 ms. Three additional NC underwent head drops at 170 ms, 370 ms, 470 ms and 570 ms to determine response latencies with precision. In NC, the short-latency response to head drops timed 170 to 470 ms after an R-spike was to shorten the time to the next R-spike in comparison to pre-drop heartbeat cycles. Drops at 570 ms delay shortened only the succeeding post-stimulus RR-interval. In LDS, head drops timed 170 ms after a heartbeat failed to shorten the ongoing cardiac cycle. For both delays only the succeeding cardiac cycle was significantly shortened. In all subjects, SP rose slightly by approximately 1-3% and BF decreased by 7-24% after 3-4 heartbeats post-drop. The results are evidence for an excitatory vestibulo-cardiac reflex in man which accelerates heart rate at a latency circa 500-600 ms. SP and BF are affected at longer latencies of several heart beats. A delayed increase of heart rate in response to postural challenge may contribute to the autonomic distress experienced by patients with vestibular loss.

Acceleration↗
PubMedDate not supplied

Migrainous vertigo: mutation analysis of the candidate genes CACNA1A, ATP1A2, SCN1A, and CACNB4.

BACKGROUND: Migrainous vertigo (MV) is increasingly recognized as a common cause of episodic vertigo. MV displays several clinical similarities with familial hemiplegic migraine (FHM) and episodic ataxia type 2 (EA-2), which have been linked to mutations in 3 genes, CACNA1A, encoding a neuronal calcium channel alpha subunit, ATP1A2, encoding a catalytic subunit of a Na(+)/K(+)-ATPase, and most recently the voltage-gated sodium channel SCN1A. The present study explored the hypothesis that mutations in CACNA1A, ATP1A2, SCN1A, and the calcium channel beta(4) subunit CACNB4 confer susceptibility to MV. METHODS: Mutation analysis of the coding exons and exon/intron junctions of CACNA1A, ATP1A2, SCN1A, and CACNB4 was performed in 14 unrelated MV patients by conformation sensitive gel electrophoresis and automated sequence analysis. RESULTS: Analysis of the 4 candidate genes in the 14 MV patients resulted in the identification of a total of 26 sequence variants. The silent substitution D29D in CACNB4 was observed in 2 MV patients and was not present in 46 ethnically matched control DNA samples. The remaining variants were also observed in control DNA samples and the allele frequencies of variants that resulted in amino acid substitutions were not significantly different between patients and controls. CONCLUSIONS: Based on this group of patients there is no evidence that the genes causing FHM and EA-2 represent major susceptibility loci for MV.

Adolescent↗